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The Blog "Beautiful Mind" contain post related to therapies, genetic analysis and prognosis related to neurological disorders and cognition.

Vivek Misra
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  • May 20, 2013
  • 01:23 PM
  • 24 views

Epilepsy Service Organization in Countries with Limited Resources

by Vivek Misra in Beautiful Mind

tumblr: bellapaige88On average, 9.5/1000 population has epilepsy in Low and Middle Income Countries (LAMIC). A research which has resulted in the global campaign against epilepsy has shown, the gap between treatment need and the treatment provision worldwide is approximately 70% [1]. This large ‘treatment gap’, i.e., lack of appropriate treatment for a large number of patients with epilepsy, due to a number of causes including inability to identify cases, inability to deliver adequate treatment, people’s attitudes and perception, availability of anti-epileptic drugs and finally, health policies of individual countries and the priority given to epilepsy. [2]The first step towards narrowing the treatment gap is improving diagnosis. Clinical investigations that help in the diagnosis of epilepsy include electroencephalography (EEG), neuro-imaging techniques such as computed axial tomograpy (CT) and magentic resonance imaging (MRI). Simple blood tests, including haematological, liver and kidney function profiles can reveal treatable causes of epilepsy, such as parasitic infections. Neuropsychological evaluation identifies areas of function and dysfunction. Long term video monitoring can greatly improve the diagnosis of epilepsy. Therapeutic drug monitoring can ensure that patients are receiving optimal doses of medication and can help greatly in avoiding toxicity. However, the availability of investigative procedures varies greatly, from 82.4% for EEG, 70.5% for CT, 45% for therapeutic drug monitoring  to only 20.6 % for MRI, 21.7% for long-term video monitoring and in LAMICs. Special investigations of brain function such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) are not available in most LAMIC centres.Epilepsy services in low and middle income countries are almost non-existent and service organization is a challenge. Epilepsy services should be community based and it is important to integrate these services into the primary health care structure to ensure sustainability. The Indian model is one such example, where epilepsy care has been incorporated into programmes for poverty alleviation [3]. Public-private partnerships and non-governmental organizations (NGO) are also important components of the Indian model. [4]The ultimate goal of all workers in the epilepsy field is to improve the quality of the life of people with epilepsy and their families. The prime manner in which this is aimed for is by the provision of good medical care.Wang WZ, Wu JZ, Wang DS, Dai XY, Yang B, Wang TP, Yuan CL, Scott RA, Prilipko LL, de Boer HM, & Sander JW (2003). The prevalence and treatment gap in epilepsy in China: an ILAE/IBE/WHO study. Neurology, 60 (9), 1544-5 PMID: 12743252Mbuba CK, Ngugi AK, Newton CR, & Carter JA (2008). The epilepsy treatment gap in developing countries: a systematic review of the magnitude, causes, and intervention strategies. Epilepsia, 49 (9), 1491-503 PMID: 18557778 Pal, D., Das, T., & Sengupta, S. (2000). ... Read more »

Mbuba CK, Ngugi AK, Newton CR, & Carter JA. (2008) The epilepsy treatment gap in developing countries: a systematic review of the magnitude, causes, and intervention strategies. Epilepsia, 49(9), 1491-503. PMID: 18557778  

Pal, D., Das, T., & Sengupta, S. (2000) Case-control and qualitative study of attrition in a community epilepsy programme in rural India. Seizure, 9(2), 119-123. DOI: 10.1053/seiz.1999.0357  

Mani KS, Rangan G, Srinivas HV, Srindharan VS, & Subbakrishna DK. (2001) Epilepsy control with phenobarbital or phenytoin in rural south India: the Yelandur study. Lancet, 357(9265), 1316-20. PMID: 11343735  

Wang WZ, Wu JZ, Wang DS, Dai XY, Yang B, Wang TP, Yuan CL, Scott RA, Prilipko LL, de Boer HM.... (2003) The prevalence and treatment gap in epilepsy in China: an ILAE/IBE/WHO study. Neurology, 60(9), 1544-5. PMID: 12743252  

  • May 10, 2013
  • 02:41 AM
  • 48 views

Mitochondrial Disease – A Neurological Perspective

by Vivek Misra in Beautiful Mind

Defects of mitochondrial function have been identified in several neurodegenerative diseases. These include abnormalities induced by mutations of mitochondrial DNA (mtDNA) those caused by mutation of nuclear genes encoding mitochondrial proteins, and in some cases, exposure to mitochondrial toxins.MtDNA mutation are associated with a variety of progressive encephalomyopathies inn which there is evidence of neurodegeneration. These include  Kearns-Sayre syndrome myopathy, encephalopathy, lactic acidosis and stroke – like episodes (MELAS) and Myoclonic epilepsy with ragged red fibers (MERRF) and Leigh’s syndrome. In Leber’s heredity optic neuropathy (LHON), there is degeneration of retinal ganglion cells. Occasional reports have described mtDNA mutation in association with Parkinson’s Diseases (PD) and amyotrophic lateral sclerosis (ALS).Mutation in the nuclear gene for mtDNA polymerase gamma (POLG) have been found in a range of disorders that include Alper’s Syndrome, progressive external opthalmoplegia (PEO), sensory ataxia, neuropathy, dysarthria and ophthalmoplegia (SANDO) and parkinsonism. Although most cases of Parkinsonism due to POLG mutations have been preceded by PEO, some have been described with only Parkinsonism and neuropathy. The early onset from hepatocerebral mtDNA depletion is associated with mutation in the deoxyguanosine  kinase gene and thymidine phosphorylase mutation are a cause of mitochondrial neurogastrointestinal  encephalomyopathy (MNGIE). Mutation have been identified in nuclear genes for mitochondrial protein involved in the assembly and maintenance of cytochrome oxidase including SCO2, SURF1, COX10, COX15 and LRPPRC. These results in autosomal recessive COX deficiency that usually presents in early life with Leigh syndrome, myopathy and encephalopathy, lactic acidosis and a progressive course with early death.There is deficiency in complex I activity in PD substantia nigra and platelets. Complex I is the target of toxin known to produce parkinsonian features in human e.g. MPTP and anonnacin, and animal model of PD e.g. rotenone and tetrahydroisoquinoline. The pathogenesis of PD also includes protein aggregation (Lewy bodies). Mitochondrial dysfunction will contribute to dysfunction of the energy dependent ubiquitin proteasomal system (UPS) and oxidative stress will add to the substrate load. Several of the single gene mutation causing familial PD has been identified as mitochondrial proteins including PINK1, DJ1 and parkin. The cellular disruption of the latter appears to depend upon the stage of cell differentiation. A proportion of LRRK2 is associated with the outer mitochondrial membrane. Mitochondrial dysfunction has also been identifies in AD, ALS and Huntington’s diseases although the relationship to pathogenesis in the respective diseases remain unknown. McFarland R, Taylor RW, & Turnbull DM (2010). A neurological perspective on mitochondrial disease. Lancet neurology, 9 (8), 829-40 PMID: 20650404Venna N (2004). Mitochondrial neurological diseases: a clinician's perspective. Neurology India, 52 (3), 305-6 PMID: 15472416... Read more »

McFarland R, Taylor RW, & Turnbull DM. (2010) A neurological perspective on mitochondrial disease. Lancet neurology, 9(8), 829-40. PMID: 20650404  

Venna N. (2004) Mitochondrial neurological diseases: a clinician's perspective. Neurology India, 52(3), 305-6. PMID: 15472416  

  • May 7, 2013
  • 12:19 PM
  • 45 views

"Insight" in Neuropsychiatric Disorders

by Vivek Misra in Beautiful Mind

photo:  jagaro.netLack of awareness of illness, poor insight or ‘denial’ are regarded as fundamental problems in neurology and psychiatry. The ‘object’ of the awareness differs in different conditions. For example a stroke patient may deny their hemiplegia (anosognosia) – a deficit which is visible and objective; a person with Alzheimer’s disease may be unaware of memory problems – which though measurable, are not readily apparent to the observer. Finally, a schizophrenic patient with hallucinations may or may not accept that the ‘voices’ that they alone hear are part of a mental illness. In neuropsychiatry the discrepancy between the patients’ and the relatives’ ratings provide a useful measure of ‘insight’. In psychiatry, it is more common to use a clinician rating and to consider separate domains.  It has been have suggested that insight in psychosis concerns 3 domains: (1) awareness of mental disorder, (2) ability to re-label psychotic phenomena as pathological, (3) compliance with treatment. This last dimension is obviously important clinically. One question for research is whether these different types of lack of awareness share a common aetiology. Within schizophrenia, insight appears to be correlated with general intellectual functioning. However, this does not explain why many patients are able to detect signs of mental disorder in another person but not themselves. There is some evidence that additional executive or ‘frontal lobe’ deficits contribute to lack of insight. More recently neuroimaging studies using MRI and voxel-based morphometric techniques have shown areas of reduced grey matter density that correlate with loss of various components of insight. Hence insight in psychiatry and neurology has come together thanks to advances in brain imaging.Pijnenborg GH, van Donkersgoed RJ, David AS, & Aleman A (2013). Changes in insight during treatment for psychotic disorders: a meta-analysis. Schizophrenia research, 144 (1-3), 109-17 PMID: 23305612... Read more »

Pijnenborg GH, van Donkersgoed RJ, David AS, & Aleman A. (2013) Changes in insight during treatment for psychotic disorders: a meta-analysis. Schizophrenia research, 144(1-3), 109-17. PMID: 23305612  

  • April 24, 2013
  • 02:58 AM
  • 74 views

Recent Trauma and Acute Infection Linked with Stroke In Children

by Vivek Misra in Beautiful Mind

Research has demonstrated that experiencing head or neck trauma or minor acute infections such as influenza can increase risk for stroke among adults. Inflammation in the CNS or in the periphery may be a risk factor for the initial development of cerebral ischemia. Fullerton (University of California, San Francisco, USA) and colleagues hypothesized that trauma and acute infections are independently associated with childhood arterial ischemic stroke (AIS). Researchers carried out a case-control study of 126 children who were admitted to hospital with AIS and 378 age- and primary care facility-matched controls. All the children were selected from a cohort of 2.5 million children and adolescents aged 19 years or younger who were enrolled in the Kaiser Permanente Medical Care Program.As reported in the Annals of Neurology, the team found that children who had medical treatment for head or neck trauma within the previous 12 weeks had a 7.5-fold increased risk for AIS compared with those who had not.The median time to stroke following head or neck trauma was short, at a median of 0.5 days, and when trauma exposure was redefined as being within the past week, the increased risk for AIS was much greater, at 39 times the risk among children who had not experienced trauma during this period.Similarly, seeking treatment for a minor infection such as upper respiratory tract infection, acute otitis media, or acute gastroenteritis within the previous 4 weeks also increased the risk for AIS 4.6-fold compared with having no infection over this time. Overall, 33% of children who had AIS had a history of infection over the previous month compared with 13% of controls.Atherosclerosis, the pathologic process underlying most coronary artery disease and the majority of ischemic stroke in humans, is an inflammatory process. Inflammatory conditions such as giant cell arteritis and systemic lupus erythematosus predispose to stroke, as do a range of acute and chronic infections, principally respiratory.  Previous studies also demonstrated that HIV infection is associated with an increased risk of stroke, particularly cerebral infarction in young patients. This risk is probably mediated by increased susceptibility of HIV-infected patients to meningitis and protein S deficiency. Diverse mechanisms have been proposed to account for inflammation and infection-associated stroke, ranging from classic risk factors to disturbances of the immune and coagulation systems.Such studies suggest that trauma and acute infection could be used as "targets for primary stroke prevention strategies and considerable opportunities therefore exist for the development of novel therapies.Hills, N., Johnston, S., Sidney, S., Zielinski, B., & Fullerton, H. (2012). Recent trauma and acute infection as risk factors for childhood arterial ischemic stroke Annals of Neurology, 72 (6), 850-858 DOI: 10.1002/ana.23688 Emsley, H., & Tyrrell, P. (2002). Inflammation and Infection in Clinical Stroke Journal of Cerebral Blood Flow & Metabolism, 1399-1419 DOI: 10.1097/00004647-200212000-00001Qureshi, A., Janssen, R., Karon, J., Weissman, J., Akbar, M., Safdar, K., & Frankel, M. (1997). Human Immunodeficiency Virus Infection and Stroke in Young Patients ... Read more »

Hills, N., Johnston, S., Sidney, S., Zielinski, B., & Fullerton, H. (2012) Recent trauma and acute infection as risk factors for childhood arterial ischemic stroke. Annals of Neurology, 72(6), 850-858. DOI: 10.1002/ana.23688  

Emsley, H., & Tyrrell, P. (2002) Inflammation and Infection in Clinical Stroke. Journal of Cerebral Blood Flow , 1399-1419. DOI: 10.1097/00004647-200212000-00001  

Qureshi, A., Janssen, R., Karon, J., Weissman, J., Akbar, M., Safdar, K., & Frankel, M. (1997) Human Immunodeficiency Virus Infection and Stroke in Young Patients. Archives of Neurology, 54(9), 1150-1153. DOI: 10.1001/archneur.1997.00550210078016  

  • April 15, 2013
  • 03:27 PM
  • 78 views

Brain-to-Brain Interface - Share Information via Internet

by Vivek Misra in Beautiful Mind

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Pais-Vieira, M., Lebedev, M., Kunicki, C., Wang, J., & Nicolelis, M. (2013) A Brain-to-Brain Interface for Real-Time Sharing of Sensorimotor Information. Scientific Reports. DOI: 10.1038/srep01319  

  • March 13, 2013
  • 02:40 AM
  • 267 views

Brain Lateralization - Logical Left vs Creative Right

by Vivek Misra in Beautiful Mind

Broad generalizations are often made in popular psychology about one side or the other having characteristic labels, such as "logical" for the left side or "creative" for the right. These labels need to be treated carefully; although a lateral dominance is measurable, both hemispheres contribute to both kinds of processes.In psychology and neurobiology, the theory is based on what is known as the lateralization of brain function. So does one side of the brain really control specific functions? Are people either left-brained or right-brained? Like many popular psychology myths, this one has a basis in fact that has been dramatically distorted and exaggerated.Language functions such as grammar, vocabulary and literal meaning are typically lateralized to the left hemisphere, especially in right handed individuals. Although 95% of right-handed people have left-hemisphere dominance for language, 18.8% of left-handed people have right-hemisphere dominance for language function. Additionally, 19.8% of the left-handed have bilateral language functions. Even within various language functions (e.g., semantics, syntax, prosody), degree (and even hemisphere) of dominance may differ. The processing of visual and auditory stimuli, spatial manipulation, facial perception, and artistic ability are represented bilaterally, but may show right hemisphere superiority. Numerical estimation, comparison and online calculation depend on bilateral parietal regions while exact calculation and fact retrieval are associated with left parietal regions, perhaps due to their ties to linguistic processing.  Dyscalculia is a neurological syndrome associated with damage to the left temporo-parietal junction. This syndrome is associated with poor numeric manipulation, poor mental arithmetic skill, and the inability to either understand or apply mathematical concepts. The right brain-left brain theory grew out of the work of Roger W. Sperry, who was awarded the Nobel Prize in 1981. While studying the effects of epilepsy, Sperry discovered that cutting the corpus collosum could reduce or eliminate seizures.However, these patients also experienced other symptoms after the communication pathway between the two sides of the brain was cut. For example, many split-brain patients found themselves unable to name objects that were processed by the right side of the brain, but were able to name objects that were processed by the left-side of the brain. Based on this information, Sperry suggested that language was controlled by the left-side of the brain.Depression is linked with a hyperactive right hemisphere, with evidence of selective involvement in "processing negative emotions, pessimistic thoughts and unconstructive thinking styles", as well as vigilance, arousal and self-reflection, and a relatively hypoactive left hemisphere, "specifically involved in processing pleasurable experiences" and "relatively more involved in decision-making processes". Additionally, "left hemisphere lesions result in an omissive response bias or error pattern whereas right hemisphere lesions result in a commissive response bias or error pattern." The delusional misidentification syndromes, reduplicative paramnesia and Capgras delusion are also often the result of right hemisphere lesions. There is evidence that the right hemisphere is more involved in processing novel situations, while the left hemisphere is most involved when routine or well-rehearsed processing is called for. Later research has shown that the brain is not nearly as dichotomous as once thought. For example, recent research has shown that abilities in subjects such as math are actually strongest when both halves of the brain work together.Taylor, I. & Taylor, M. M. (1990). Psycholinguistics: Learning and using Language. Pearson. ISBN 978-0-13-733817-7. p. 367Beaumont, J.G. (2008). Introduction to Neuropsychology, Second Edition. The Guilford Press. ISBN 978-1-59385-068-5. Chapter 7Ross, E., & Monnot, M. (2008). Neurology of affective prosody and its functional–anatomic organization in right hemisphere Brain and Language, 104 (1), 51-74 DOI: 10.1016/j.bandl.2007.04.007... Read more »

Ross, E., & Monnot, M. (2008) Neurology of affective prosody and its functional–anatomic organization in right hemisphere. Brain and Language, 104(1), 51-74. DOI: 10.1016/j.bandl.2007.04.007  

George MS, Parekh PI, Rosinsky N, Ketter TA, Kimbrell TA, Heilman KM, Herscovitch P, & Post RM. (1996) Understanding emotional prosody activates right hemisphere regions. Archives of neurology, 53(7), 665-70. PMID: 8929174  

Dehaene, S. (1999) Sources of Mathematical Thinking: Behavioral and Brain-Imaging Evidence. Science, 284(5416), 970-974. DOI: 10.1126/science.284.5416.970  

Dehaene, S., Piazza, M., Pinel, P., & Cohen, L. (2003) THREE PARIETAL CIRCUITS FOR NUMBER PROCESSING. Cognitive Neuropsychology, 20(3-6), 487-506. DOI: 10.1080/02643290244000239  

Hecht, D. (2010) Depression and the hyperactive right-hemisphere. Neuroscience Research, 68(2), 77-87. DOI: 10.1016/j.neures.2010.06.013  

Devinsky, O. (2009) Delusional misidentifications and duplications: Right brain lesions, left brain delusions. Neurology, 72(1), 80-87. DOI: 10.1212/01.wnl.0000338625.47892.74  

  • February 24, 2013
  • 05:23 PM
  • 211 views

Drugs, Dopamine and Drosophila: A Fly Model for ADHD?

by Vivek Misra in Beautiful Mind

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Lebestky T, Chang JS, Dankert H, Zelnik L, Kim YC, Han KA, Wolf FW, Perona P, & Anderson DJ. (2009) Two different forms of arousal in Drosophila are oppositely regulated by the dopamine D1 receptor ortholog DopR via distinct neural circuits. Neuron, 64(4), 522-36. PMID: 19945394  

Wang L, & Anderson DJ. (2010) Identification of an aggression-promoting pheromone and its receptor neurons in Drosophila. Nature, 463(7278), 227-31. PMID: 19966787  

  • January 11, 2013
  • 10:31 AM
  • 89 views

“Gantenerumab” could pave way for Alzheimer's treatment

by Vivek Misra in Beautiful Mind

An experimental drug being developed by Roche Holding AG removed amyloid plaques from the brains of Alzheimer's disease patients in a small early-stage study, according to data published in the Archives of Neurology, Oct 10.Many researchers suspect the build-up of such plaques may be a cause of the memory robbing disease, although that theory has yet to be definitively proved.The next step will be to investigate whether removal of brain amyloid translates into clinical benefit for patients at doses of the experimental drug, gantenerumab, that are well tolerated and safe.Gantenerumab, a biotech drug designed to bind to amyloid plaques in the brain and remove them, is being targeted at the early stages of Alzheimer's with the hope it can slow progression of the disease while patients are still able to function.Passive ImmunotherapyAdministering gantenerumab circumvents stimulation of the adaptive immune system and ensures adequate antibody exposure in the Alzheimer’s patient.The study included data from 16 AD patients, aged 50 to 90 years, who were included in a positron emission tomographic (PET) substudy of a larger multiple ascending dose trial.For inclusion in the study the patients must have probable AD according to the National Institute of Neurological Disorders and Stroke – Alzheimer’s Disease and Related Disorders Association criteria, a Mini-Mental State Examination Score between 16 and 26 (inclusive), a magnetic resonance imaging (MRI) scan consistent with AD, and a modified Hachinski ischemia score of 4 or less.APOE genotyping was performed for all patients.The patients were assigned to receive intravenous infusions of gantenerumab (60 mg, n = 6; 200 mg, n = 6) or placebo (n = 4) once every 4 weeks to a total of 7 infusions, but because of early termination of dosing in the 200-mg gantenerumab group, not all participants received 7 infusions.In the 60-mg group, all patients received 7 infusions, while in the 200-mg group 1 patient received 5 infusions, 2 patients received 4 infusions, 2 patients received 3 infusions, and 1 patient received 2 infusions.In the placebo group, 2 patients received all 7 infusions, 1 patient received 5 infusions, and 1 patient received 2 infusions.Baseline images were compared with images obtained at the end of treatment to determine the change in brain amyloid, as measured by carbon 11-labeled Pittsburgh compound B PET.Additionally, to evaluate gantenerumab’s ability to clear amyloid plaques via phagocytosis, primary microglial cells obtained from healthy human brain tissue during tumor surgery were incubated in different concentrations of the drug.The study found a mean percentage reduction from baseline in cortical brain amyloid relative to placebo of 15.6% in the 60-mg group and 35.7% in the 200-mg group.Findings in the placebo group support previous reports that "amyloid load continues to increase in many patients with mild-to-moderate AD," the authors added.MicrohemorrhageTwo patients treated with gantenerumab, both of them APOE ε4 homozygous, showed abnormalities on MRI fluid-attenuated inversion recovery (FLAIR) imaging that were "consistent with inflammation or vasogenic edema" after 2 and 4 of the 200-mg doses.Both patients also developed microhemorrhages, and 1 was "mildly symptomatic" with headaches, dizziness, gait instability, and tremor, the investigators reported.These adverse effects resolved spontaneously after discontinuation of dosing, similar to what has been reported after treatment with bapineuzumab.The FLAIR abnormalities were most conspicuous in areas of more prominent amyloid reduction and "may be seen as instances of excessive pharmacological activity due to a high dose or more susceptible individuals (e.g., carriers of the APOE ε4 genotype).However, according to the researchers, a smaller reduction in amyloid was seen with no FLAIR abnormalities at a lower dose of gantenerumab.This suggests that gantenerumab-induced amyloid lowering can be achieved without significantly perturbing vascular permeability through inflammation or blockage of Aβ clearance pathways when appropriate dosing is selected.Much larger trials and further study will be needed to fully understand just how gantenerumab works and whether it can stave off Alzheimer's disease.Early, or prodromal, Alzheimer's disease is a condition in which a person's memory loss is worse than can be expected by the normal aging process, while their ability to engage in daily activities is not affected to the extent that dementia would be diagnosed.Alzheimer's disease is estimated to affect 25 million people around the world, with the number of diagnosed cases expected to rise dramatically with the aging of the enormous baby boom generation.It is expected that the illness, which robs memory and ability to function, will affect about 63 million people by 2030, and 114 million by 2050 worldwide, according to forecasts cited by Roche.... Read more »

Ostrowitzki, S., Deptula, D., Thurfjell, L., Barkhof, F., Bohrmann, B., Brooks, D., Klunk, W., Ashford, E., Yoo, K., Xu, Z.... (2011) Mechanism of Amyloid Removal in Patients With Alzheimer Disease Treated With Gantenerumab. Archives of Neurology, 69(2), 198-207. DOI: 10.1001/archneurol.2011.1538  

  • January 11, 2013
  • 10:14 AM
  • 145 views

"Alarm clock" gene explains wake-up function of biological clock

by Vivek Misra in Beautiful Mind

Tring Tring.....Wake Up...Its Morning...Mr. V :  I didn't set an alarm !!! whose this ???Ever wondered why you wake up in the morning—even when the alarm clock isn't making jarring noises? Researchers at the Salk Institute for Biological Studies have identified a new component of the biological clock, a gene responsible for starting the clock from its restful state every morning.The biological clock ramps up our metabolism early each day, initiating important physiological functions that tell our bodies that it's time to rise and shine. Discovery of this new gene and the mechanism by which it starts the clock everyday may help explain the genetic underpinnings of sleeplessness, aging and chronic illnesses, such as cancer and diabetes, and could eventually lead to new therapies for these illnesses.In a report published in September, 29 in the journal Science, the Salk researchers and their collaborators at McGill University and Albert Einstein College of Medicine describe how the gene KDM5A encodes a protein, JARID1a, that serves as an activation switch in the biochemical circuit that maintains our circadian rhythm.The discovery fills in a missing link in the molecular mechanisms that control our daily wake-sleep cycle. The central player of our biological clock is a protein called PERIOD (PER). The number of PER proteins in each of our cells rises and falls every 24 hours. Our cells use the level of PER protein as an indicator of the time of the day and tell our body when to sleep or be awake.As we already know about two genes CLOCK and BMAL1, served as the key drivers for raising PER protein levels. As the level of PER protein rises during the daytime, reaching its peak around evening, it somehow puts a break on CLOCK and BMAL, thereby reducing its own level during nighttime.Falling PER protein levels at night causes our biological systems to slow: our blood pressure drops, our heart rate slows and our mental processes wind down. But, until now, the precise nature of the nighttime brake and what let CLOCK and BMAL proteins overcome this brake to raise PER protein levels again each morning was a mystery.In their research, which was primarily funded by Salk's Innovation Fund, Panda and his colleagues identified JARID1a, a type of enzyme, as the molecular bugle call for cells and organs to get back to work each morning. By studying the genetic mechanisms underlying circadian rhythms in human and mouse cells and in fruit flies, the researchers discovered that JARID1a was required for normal cycling, both at the cellular level and in terms of an organisms' daily behavior.In human and mouse cells that were genetically modified to under-produce JARID1a, the PER protein did not rise to its normal peak each day. Fruit flies that were similarly genetically altered also had low levels of PER protein. The flies lost track of time: they did not know when to sleep or wake up and took frequent naps throughout the day and night.Digging deeper into the molecular workings of the clock, Panda and his colleagues found that each morning, JARID1a reactivates CLOCK and BMAL1 by countering the action of a brake protein HDAC1. They suspect PER protein tells HDAC1 to put a brake on its own production at night. "JARID1a tells that break to ease off, which causes CLOCK and BMAL1 drivers to rev back up every morning," Panda says.To support their findings about the clock's workings, the researchers studied genetically altered mice cells and fruit flies that lacked the JARID1a gene. They inserted JARID1a into the flies' DNA, which released the HDAC brake so the flies returned to a normal cycle. They treated mouse cells with a drug that mimics JARID1a, which allowed their biological clocks to operate normally.Now that scientists understand why we wake each day, they can explore the role of JARID1a in sleep disorders and chronic diseases, possibly using it as a target for new drugs. With age, for instance, the biological clock seems to decline, often causing older people to suffer from difficulty sleeping. There is also strong evidence that shift workers, such as nurses and emergency personnel, who work long shifts that break them out of the normal 24-hour cycle of waking and sleeping, are at much higher risk for certain diseases. The cellular mechanisms of diabetes, another chronic disease, are also tied to metabolic cycles controlled by the biological clock. For instance, the conversion of sugars into fat, which normally occurs only at certain times of day, often seems to take place all day long in diabetics' bodies, suggesting the clock has lost control."So much of what it means to be healthy and youthful comes down to a good night's sleep," Panda says. "Now that we have identified JARID1a in activating our daytime cycle, we have a whole new avenue to explore why some people's circadian rhythms are off and to perhaps find new ways to help them."DiTacchio, L., Le, H., Vollmers, C., Hatori, M., Witcher, M., Secombe, J., & Panda, S. (2011). Histone Lysine Demethylase JARID1a Activates CLOCK-BMAL1 and Influences the Circadian Clock Science, 333 (6051), 1881-1885 DOI: 10.1126/science.1206022 ... Read more »

DiTacchio, L., Le, H., Vollmers, C., Hatori, M., Witcher, M., Secombe, J., & Panda, S. (2011) Histone Lysine Demethylase JARID1a Activates CLOCK-BMAL1 and Influences the Circadian Clock. Science, 333(6051), 1881-1885. DOI: 10.1126/science.1206022  

  • January 11, 2013
  • 06:52 AM
  • 243 views

Is it the Type of Pencil or Really my Handwriting is Illegible !!!

by Vivek Misra in Beautiful Mind

It is quite obvious for a 4th grader to pass the buck for his/her bad handwriting. Recently, I came across some "real research articles" published in indexed journals addressing the same.Research indicates, it should be the type of pencil which should be blamed for legibility and speed in various writing task which include cursive writing, 10-min copy task, etc or maybe not !!!Conclusion 1: Results indicate that although the students in this study wrote more legibly on the short task than on the long task, the type of grasp they used did not affect their legibility. Because of the limited sample size, the results of this study should be interpreted cautiously. More research in handwriting performance and pencil grasp is needed to provide clear expectations and treatment options for students.Conclusion 2: Study found the lateral quadrupod and four-finger pencil grips to be as functional as the dynamic tripod, lateral tripod, and dynamic quadrupod pencil grips. Study also provided average handwriting speeds for fourth-grade students on the ETCH-C.Conclusion 3: The quality of the handwriting decreased after the 10-minute copy task; however, there was no difference in the quality or speed scores among the different pencil grasps before and after the copy task. The dynamic tripod pencil grasp did not offer any advantage over the lateral tripod or the dynamic or lateral quadrupod pencil grasps in terms of quality of handwriting after a 10-minute copy task. These four pencil grasp patterns performed equivalently. Findings did questioned about the practice of having students adopt the dynamic tripod pencil grasp.  Schwellnus H, Carnahan H, Kushki A, Polatajko H, Missiuna C, & Chau T (2012). Effect of pencil grasp on the speed and legibility of handwriting after a 10-minute copy task in Grade 4 children. Australian occupational therapy journal, 59 (3), 180-7 PMID: 22690768Koziatek SM, & Powell NJ (2003). Pencil grips, legibility, and speed of fourth-graders' writing in cursive. The American journal of occupational therapy : official publication of the American Occupational Therapy Association, 57 (3), 284-8 PMID: 12785666Dennis JL, & Swinth Y (2001). Pencil grasp and children's handwriting legibility during different-length writing tasks. The American journal of occupational therapy : official publication of the American Occupational Therapy Association, 55 (2), 175-83 PMID: 11761133... Read more »

Schwellnus H, Carnahan H, Kushki A, Polatajko H, Missiuna C, & Chau T. (2012) Effect of pencil grasp on the speed and legibility of handwriting after a 10-minute copy task in Grade 4 children. Australian occupational therapy journal, 59(3), 180-7. PMID: 22690768  

Koziatek SM, & Powell NJ. (2003) Pencil grips, legibility, and speed of fourth-graders' writing in cursive. The American journal of occupational therapy : official publication of the American Occupational Therapy Association, 57(3), 284-8. PMID: 12785666  

Dennis JL, & Swinth Y. (2001) Pencil grasp and children's handwriting legibility during different-length writing tasks. The American journal of occupational therapy : official publication of the American Occupational Therapy Association, 55(2), 175-83. PMID: 11761133  

  • September 26, 2012
  • 03:51 AM
  • 362 views

HIV and Cognition: Indian Perspective

by Vivek Misra in Beautiful Mind

Dementia, as we all knows about it as an aging problem, which strikes the elderly people in society. When we look upon the Indian population, we can say that we are very young as 50% of our population is under forty years of age. As compared to developed countries, we have low prevalence and incidence rate of dementia.When we look upon neuro-infection and dementia, we find four major classes of neuro-infection related to dementia.1. Chronic Meningitis – Neurotuberculosis, fungal dementia, cryptococcal dementia, candidiasis, coccidiodomycosis, parasitic dementia and Neurocysticercosis.2. Neurosyphilis – Tertiary Syphilis, Dementia paralytica and general paresis of the insane.3. AIDS related Dementia – HIV encephalopathy, AIDS dementia complex and minor cognitive impairment. 4. Other infection includes whipple’s diseases and lyme diseases.Special features of HIV/AIDS in IndiaIn India, predominantly due to HIV C1 with very rare recombinant strains. Mode of transmission is mainly unprotective heterosexual intercourse about 85%, where contribution of homosexuality is negligible. Blood transfusion results in about 2.3% of all HIV cases. Of all the neuro-AIDS cases, neurological manifestation, opportunistic neuro-infection constitutes about 70-85%. In addition, HIV associated neoplasia are infrequent including primary lymphoma. HIV associated Dementia and HIV encephalitis are less common. Spinal pathology including vacuolar myelopathy is rare. Kaposi Sarcoma has not been reported in Indian population.According to a study  conducted at National Institute of Mental Health and Neurosciences (NIMHANS), the Neuropsychiatric clinic has registered more than one thousand five hundred cases over last 20 years, which sums up to 150cases/year, which is a very large proportion. In the opportunistic neuro-infection associated with HIV/AIDS the major infection are Cryptococcal (32.2%) followed by Neurotuberculosis (31.9%). But, when we see the prevalence of HIV/AIDS Dementia it is only 1.4%. On comparing the data with developed countries, the difference found is just 2-4% in all categories except in case of dementia, which varies from 30-40% in western countries. This is a glaring difference and special feature of HIV/AIDS in India with context to other parts of the world.While overviewing neurocognitive disorder in HIV, there are various types of manifestation i.e. 1. AIDS Dementia Complex also known as HIV associated cognitive motor complex or HIV associated dementia. 2. Minor cognitive impairment. 3. Asymptomatic neurocognitive disorder. When we look upon the therapeutic scenario for HIV/AIDS Dementia, after the introduction of Highly Active Antiretroviral Therapy (HAART) it reduced the prevalence percentage to almost half of its original both in India and worldwide.Effects of HIV associated Neurocognitive disorderThe neurological conditions can manifest as behavioral changes such are apathy, irritability, psychomotor retardation and even some patients develop manic symptoms. Whereas the symptoms associated with HIV dementia are very distinct, these include Sub-cortical dementia, which affect the working memory eg. Short term memory, executive functions such as planning and cognition eg abstract thinking, initiating an action. When we analyze HIV associated dementia (HAND), we found several risk factors, and those include Effects of Substance Abuse, Opiod Substitution Therapy, Traumatic Brain Injury, Mental Illness, Sexual Risk Behavior, Drug Related Risk Behavior and Medication Adherence.In order to precisely evaluate the clinical trait for HAND in Indian population, National bodies collaborated and conducted four individual and cohort studies between 1989 to 2006.1. Dementia Associated with HIV : NIMHANS StudyStudy registered 1239 patients with HIV related neurological complications. Only 19(1.5) cases were diagnosed of dementia with the mean age of 36.7±9.9years with male: female was 5:1. Majority of them shows memory impairment, behavioral disturbance in the form of apathy and incontinence. Imaging techniques shows ventricular enlargement, atrophy of caudate, putamen and nucleus accumbens. Early hyper-metabolism in basal ganglia and latter condition hypo-metabolism. HIV autopsy data (N=170) shows two cases associated with dementia. The data were cross referenced with other regions in the country and they also show consistency with the prevalence of 1-4% of HIV associated dementia. So this study proposed questions like is it due to viz. early death due to opportunistic infections, under reporting, inadequate methods of evaluation, socio-cultural ethos, clade”C” vs Clade “B” virus difference or any other protective factors are include in the pathogenesis.2. HIV 1, HIV2, Co-Infection and Neurological ProgressionProf. P.Satishchandra and Dr. Mahendra Kumar of University of Miami, received a NIH RO1 project grant to conduct a 5-year prospective study to find the co-relation between the infection and neurological progression. After following the strict inclusion and exclusion criteria biochemical studies were carried out and the subjects were followed up in 6th, 18th and 30th month, where detail clinical and neurological examination, CD4 testing, psychiatric assessment and neuro-psychological assessment was carried out. Over the follow up study it has being observed that CD4 count comes down with the progression of the disease. As the disease progresses the patients develop opportunistic infection but were intact psychologically and cognitively. After this study patients were prescribed HAART due to severe symptoms.3. HIV 1 subtype CThis prospective study shows that, “there is a significant difference in the data obtained in India and in western countries.” So the question arise is it due to the HIV virus subtype? In order to investigate further, the research teams led by Dr. Satishchandra and Dr. Udaykumar start working upon TAT protein of HIV1 subtype C virus. After analyzing the protein and gene sequence it has been found that in Indian population the C virus is highly intact with very less recombinant variant and also that the C virus variant was defective for monocytic chemotactic activity. Loss of C-TAT chemotactic property may underlie reduced incidence of HIV associated dementia with HIV 1 C virus. 11,124. Impact of Neurological Opportunistic Infection on Cognition in HIV Positive Adults. Another study which was conducted at NIMHANS, aimed to find out the co-relation between neuroinfection and cognition. After reviewing the data, which postulates the following point;1. Cognitive deficits are a squeal of neuro-infection.2. Cognitive deficit are present in HIV infection but largely studied in clade B infection. 3. Cognitive deficit also occur in HIV clade C infection.To summarize we can state that, the facts which concern over HIV/NeuroAIDS and cognition include;a. Opportunistic infections commonly associated with HIV/NeuroAIDS.b. Neuological opportunistic infections (NOI) less prevalent(10-25%) in developed countries.4c. NOI more prevalent (85%) in developing countries8d. Surprisingly, all studies exclude HIV patients when they undertook study upon NOI.... Read more »

Hemelaar J, Gouws E, Ghys PD, Osmanov S, & WHO-UNAIDS Network for HIV Isolation and Characterisation. (2011) Global trends in molecular epidemiology of HIV-1 during 2000-2007. AIDS (London, England), 25(5), 679-89. PMID: 21297424  

Siddappa NB, Dash PK, Mahadevan A, Jayasuryan N, Hu F, Dice B, Keefe R, Satish KS, Satish B, Sreekanthan K.... (2004) Identification of subtype C human immunodeficiency virus type 1 by subtype-specific PCR and its use in the characterization of viruses circulating in the southern parts of India. Journal of clinical microbiology, 42(6), 2742-51. PMID: 15184461  

Satishchandra P, Nalini A, Gourie-Devi M, Khanna N, Santosh V, Ravi V, Desai A, Chandramuki A, Jayakumar PN, & Shankar SK. (2000) Profile of neurologic disorders associated with HIV/AIDS from Bangalore, south India (1989-96). The Indian journal of medical research, 14-23. PMID: 10793489  

Gupta JD, Satishchandra P, Gopukumar K, Wilkie F, Waldrop-Valverde D, Ellis R, Ownby R, Subbakrishna DK, Desai A, Kamat A.... (2007) Neuropsychological deficits in human immunodeficiency virus type 1 clade C-seropositive adults from South India. Journal of neurovirology, 13(3), 195-202. PMID: 17613709  

Ranga U, Shankarappa R, Siddappa NB, Ramakrishna L, Nagendran R, Mahalingam M, Mahadevan A, Jayasuryan N, Satishchandra P, Shankar SK.... (2004) Tat protein of human immunodeficiency virus type 1 subtype C strains is a defective chemokine. Journal of virology, 78(5), 2586-90. PMID: 14963162  

Baldewicz TT, Leserman J, Silva SG, Petitto JM, Golden RN, Perkins DO, Barroso J, & Evans DL. (2004) Changes in neuropsychological functioning with progression of HIV-1 infection: results of an 8-year longitudinal investigation. AIDS and behavior, 8(3), 345-55. PMID: 15475681  

  • September 4, 2012
  • 04:18 PM
  • 556 views

Neurocysticercosis - A Challenge for Developing Countries

by Vivek Misra in Beautiful Mind

Taenia solium. by Dr Frank GaillardCysticercosis of Brain or Neurocysticercosis is most common parasitic infection of the brain or central nervous system worldwide and the most common cause of adult onset epilepsy. The cause of human cysticercosis is the larval form of Taenia solium (pork tapeworm).Neurocysticercosis is more common in developing countries and is endemic in Mexico and Latin America, sub-Saharan Africa, India, and East Asia. According to WHO data there are 2,000,000 cases of the diseases out of which 50-70% are asymptomatic while 10-30% are symptomatic with severe disability and mortality.The disease is spread via the fecal-oral route through contaminated food and water, and is primarily a food borne disease. Patients get infected by eating undercooked pork that contains viable cysticerci.  After ingestion the eggs pass through the lumen of the intestine into the tissues and migrate preferentially to the brain and muscles.The progression of neurocysticercosis can be divided into four phases:1. Vesicular Phase is the initial phase where translucid membrane is viable with low inflammatory reaction. At this time patients is asymptomatic.2. Coloidal Phase, where the pathology manifest as membrane grows and parasite dies which leads to the degeneration of escolex. This condition causes severe inflammatory brain reaction resulting in seizures and comatose.3. Granular Phase, which marks by the complete degeneration of escolex and thick membrane. Severe gliosis – arachnoidits (a chronic diseases which is linked to HLA complex) reported in this phase.4. Calcified Phase, where the lesion get calcified without any inflammatory reaction. Resulting in gliosis which is the most common finding in asymptomatic population.The pathology for neurocysticercosis involves many mechanisms such as development of hydrocephalous from granular ependimytis, vascular damage from arachnoidits, edema and reactive gliosis. NCC can be classified into two categories viz Active lesion and Inactive lesion. While classifying them, two main criteria must be followed:1. Inflammatory patterns in Cerebrospinal fluid.2. Evidence of viable lesion within the brain parenchyma in imaging studies (except for calcified lesion).Treatment option for neurocysticercosis include the high drug dosage of Albendazole, Praziquantel, and Steroids such as prednisone ranging from 50mg/day in some cases for months.Neurocysticercosis and Neuropsychiatric ProblemsIn a retrospective studies it is being found that a considerable number of patients develop Language dysfunction, gait apraxia, cognitive impairment, psychosis and in some cases mental disease as primary manifestation.Before the advancement in the imaging techniques like Computerized Axial Tomography, the symptom based diagnosis is based upon number of factors viz. presence of (a) Dementia, Delirium, excitability, hallucinations; Confusion, delirium, excitability, visual and auditory hallucinations (b) Bonnet syndrome: complex visual hallucinations (c) judgment persists normal, severe confusion, stupor.But there are more than hundred causes for dementia which include degenerative disorders, hereditary, vascular diseases and CNS infectious diseases. Hence dementia based diagnosis for neurocysticercosis is not very appropriate.While over viewing the scenario of neuropsychiatry with context to neurocysticercosis, it has being found that about 87% patients suffer from cognitive disturbance while 15% patients develop severe cognitive abnormality. Also there are very few studies documented on the topic with limited sample size.The aim of the current research should be in order to find the answer for questions like;1. How many patients with NCC develop dementia?2. What are the risk factors associated with NCC and dementia?3. What is the outcome for patients with NCC + dementia after cysticide treatment?4. To confirms the role of dementia in NCC with a large set of clinical data. Sotelo J, & Del Brutto OH (2000). Brain cysticercosis. Archives of medical research, 31 (1), 3-14 PMID: 10767474Del Brutto OH, & García HH (2012). Neurocysticercosis in Nonendemic Countries: Time for a Reappraisal. Neuroepidemiology, 39 (2), 145-146 PMID: 22922488... Read more »

Sotelo J, & Del Brutto OH. (2000) Brain cysticercosis. Archives of medical research, 31(1), 3-14. PMID: 10767474  

Del Brutto OH, & García HH. (2012) Neurocysticercosis in Nonendemic Countries: Time for a Reappraisal. Neuroepidemiology, 39(2), 145-146. PMID: 22922488  

Tejado Lde A, Pozo KT, Palomino CB, & de Dios de Vega JL. (2012) Psychiatric manifestations of neurocysticercosis in paediatric patients. BMJ case reports. PMID: 22892232  

  • June 18, 2012
  • 07:11 AM
  • 824 views

Did we neglected Essential Tremor over Parkinson’s Diseases?

by Vivek Misra in Beautiful Mind

Movement Disorder. TremorParkinson’s disease (PD) and Essential Tremor (ET) both are classified under Movement Disorder. The symptoms are commonly confused with each other and patients were misdiagnosed mainly because ET is not as well known.  Over the last three decades organizations and philanthropist like Michael J. Fox Foundation, Muhammad Ali, etc spread public awareness about PD whereas, ET remain in a darkness. Because of this, ET is not as well-known to the general public even though it is as much as 20 times more prevalent than Parkinson's disease.The two disorders differ in etiology and symptoms. As of now we understand the cause of PD quite well. As, it manifests when there is a loss of about 80% of the dopaminergic neurons in substantia nigra. However, the cause behind the death of these dopaminergic neurons is still unknown. The etiology of ET is still unknown. No pathologic findings are known to be consistently associated with essential tremor. However it been hypothesized that just like PD, it involve the deep nuclei and white matter of the brain, including the thalamus and striatum and cerebellar-brainstem-thalamic-cortical circuits probably are involved. It has been also estimated that approximately one-half of the ET cases is due to a genetic mutation and the pattern of inheritance is most consistent with autosomal dominant transmission.The symptoms of PD include tremor, rigidity, akinesia, and postural instability. Bradykinesia (slowed movements) and bradyphrenia (slowed cognition) are also common symptoms. Tremors in PD (if present) mostly manifest as a resting tremor. In other words, there is less of an action tremor than a resting tremor. Emotional changes are also common; depression and facial masking (little facial expression of emotion) are particularly prevalent. ET generally presents as a rhythmic tremor which begins in one upper extremity and soon affects the other and is present only when the affected muscle is exerting effort (in other words, it is not present at rest). In about 30% of cases, tremor involves the cranial musculature; the head is involved most frequently, followed by voice, jaw, and face. Any sort of physical or mental stress will tend to make the tremor worse, often creating the false impression that the tremor is of psychosomatic origin. Both Parkinson’s diseases and Essential Tremor are generally progressive in most cases (sometimes rapidly, sometimes very slowly), and can be disabling in severe cases.  Additionally, patients with essential tremor are more likely to develop or have PD.There is no known cure for both PD and ET. The goal of treatment is to control symptoms. Treatment of PD usually starts with levodopa and anticholinergic therapy. Treatment of ET usually involves antiepileptic primidone and beta-adrenergic blocker propranolol. Deep brain stimulation (DBS) of the subthalamic nucleus, globus pallidus, or thalamus are becoming more common treatments of both essential tremor and PD. DBS was approved for treatment of ET in 1997 and for PD in 2002. While we still have a lot to learn about these two diseases, we have come a long way in understanding and treating both the diseases. However there is an immediate need to raise public awareness about Essential Tremor and its outcomes. Louis ED, Ottman R, & Hauser WA (1998). How common is the most common adult movement disorder? estimates of the prevalence of essential tremor throughout the world. Movement disorders : official journal of the Movement Disorder Society, 13 (1), 5-10 PMID: 9452318Flora ED, Perera CL, Cameron AL, & Maddern GJ (2010). Deep brain stimulation for essential tremor: a systematic review. Movement disorders : official journal of the Movement Disorder Society, 25 (11), 1550-9 PMID: 20623768... Read more »

Louis ED, Ottman R, & Hauser WA. (1998) How common is the most common adult movement disorder? estimates of the prevalence of essential tremor throughout the world. Movement disorders : official journal of the Movement Disorder Society, 13(1), 5-10. PMID: 9452318  

Flora ED, Perera CL, Cameron AL, & Maddern GJ. (2010) Deep brain stimulation for essential tremor: a systematic review. Movement disorders : official journal of the Movement Disorder Society, 25(11), 1550-9. PMID: 20623768  

  • June 10, 2012
  • 01:05 PM
  • 818 views

Stem Cells to Cure Multiple Sclerosis - From in vivo to Clinical Trials.

by Vivek Misra in Beautiful Mind

© Ectins project- by Prof. John SindenMultiple Sclerosis, also known as disseminated sclerosis, is an autoimmune disease in which the immune system attacks myelin sheaths that surround and protect nerve cells. The damage leads to demyelination and scarring which leaves the nerves exposed and unable to send signals to the brain and back, resulting in the loss of motor skills, coordination, vision, and cognitive abilities. There is no specific treatment exists for patients with MS who fails to respond to conventional immunosuppressive and immunomodulating treatment strategies, which include the use of corticosteroids, interferon and non interferon - non steroidal immunomodulator. And more recently humanized monoclonal antibody immunomodulator, natalizumab. (commercial name Tysabri)Over the last decade, Stem Cell Transplantation (SCT) has emerged as a popular potential therapeutic choice for numerous progressive autoimmune and neurological disorders. However only hematopoietic stem cells (HSC) have been studied in great detail, scientists know little about how they modulate the immune system and promote tissue repair in living organisms.According to research, published in May 20th issue of Nature Neuroscience, a growth factor produced by hMSCs fights MS in two ways: blocking a destructive autoimmune response and repairing neuronal damage. The finding could help advance ongoing clinical trials testing hMSCs as a therapy for MS. The researchers have identified a unique factor “Hepatocyte Growth Factor” (HGF) and its primary receptor cMET, has surprisingly potent activity mediating neuron repair in induced experimental autoimmune encephalomyelitis (EAE) in mouse models.In 2009, Miller’s lab. reported that hMSCs dramatically reversed the symptoms of multiple sclerosis in a mouse model of the disorder. The team hypothesized that the stem cells suppress the immune response and promote remyelination. However, the mechanism involved was not clear. To find out, team isolated the medium on which the hMSCs were grown to determine if the cells or something they secreted was responsible for the observed recovery. The medium alone was enough to induce recovery in mice, pointing to the latter.To find out exactly which molecule or molecules in the medium were responsible, the researchers separated the proteins in the fluid based on the molecular weight and injected each isolate into mice exhibiting symptoms of MS. The mid-weight solution, of proteins with masses between 50 and 100 kilodaltons (kDa), caused recovery.They identified hepatocyte growth factor (HGF), a cytokine made by mesenchymal cells that has been shown to promote tissue regeneration and cell survival in numerous experiments. Sure enough, HGF alone was enough to promote recovery in the MS mouse models, and blocking the receptor for HGF in those mice blocked recovery. The team also demonstrated that HGF suppresses immune responses in vivo and accelerates remyelination of neurons in vitro. Finally, they saw that HGF causes remyelination in rats with a lesion on their spinal cord.A clinical phase trial study published in June issue of Multiple Sclerosis Journal report that autologous HSC transplantation (AHSCT) with a BEAM/ATG conditioning regimen, help the subjects in not only slowing down the progression of diseases but also in continued clinical improvement, especially if subjects are still in the relapsing-remitting phase of the diseases. Mancardi et.al along with Italian BMT Study Group reports the long term follow-up findings from the data obtained from the European Group for Blood and Marrow Transplantation (EBMT) registry. Six centres come along to organize a phase I/II study, aimed to evaluate the outcomes of AHSCT on MRI markers. Later, the patients were subjected to BEAM/ATG conditioning regimen and outcomes were reported to EBMT registry and two leading haemato-neurological centres in Italy. The study was approved by local ethics committee and based upon EBMT guidelines.After the transplant procedure, all patients were examined every 3 months for first two years and then at least once a year in subsequent period. The study constituted of 74 patients and the median follow-up period of 48.3 (range 0.8 – 126) months. The evaluation is based upon the clinical and MRI outcomes. Transplant related mortality include early toxic effect found in 80% of total cases, which include neuropenic fever (70%), sepsis (30%), UTI (25%) and diarrhea and severe mucositis (15%). During neuropenic period related fever, transient worsening of neurological symptoms with headache, fatigue, deterioration of motor and sensory symptoms were found in 50% of cases.   The study reports that, after 5 years, two-third remained stable and shows improved outcomes. With follow up time more than 1 yr, 31% of patients with relapsing-remitting course confirmed EDS scale improvement >1 point after AHSCT when compared to 3% which have secondary progressive disease course. In seven year long follow-up of 18 subjects, 44% remained stable and sustained improvement while rest of the subjects after initial stabilization or improvement with mean period of 3.5 shows slow disability progression. There are currently several clinical trials testing the potential of Stem Cells in MS patients around the world, including a phase I trial at the Cleveland Clinic in Ohio that emerged from the work in Miller’s lab which is based upon hMSCs. The large cohorts like EBMT consistently evaluate the outcomes of hematopoietic stem cell transplantation. With the knowledge adding up which provides us with the insight behind the mechanism of stem cell therapy is like fixing up the cubes into a puzzle based upon which new therapeutic targets come into play. Whereas the measuring the outcomes from large cohort studies not only help us in evaluating the efficacy of a procedure/ clinical practice but also tells us about the hurdle they face in population, which is to be resolved in laboratory. With the results building upon, the question is “Can Stem Cells Will Be Able To Cure Multiple Sclerosis In Near Future?”     Bai L, Lennon DP, Caplan AI, Dechant A, Hecker J, Kranso J, Zaremba A, & Miller RH (2012). Hepatocyte growth factor mediates mesenchymal stem cell-induced recovery in multiple sclerosis models. Nature neuroscience PMID: 22610068Mancardi G, Sormani M, Di Gioia M, Vuolo L, Gualandi F, Amato M, Capello E, Currò D, Uccelli A, Bertolotto A, Gasperini C, Lugaresi A, Merelli E, Meucci G, Motti L, Tola M, Scarpini E, Repice A, Massacesi L, Saccardi R, & the Italian BMT S... Read more »

Bai L, Lennon DP, Caplan AI, Dechant A, Hecker J, Kranso J, Zaremba A, & Miller RH. (2012) Hepatocyte growth factor mediates mesenchymal stem cell-induced recovery in multiple sclerosis models. Nature neuroscience. PMID: 22610068  

Mancardi G, Sormani M, Di Gioia M, Vuolo L, Gualandi F, Amato M, Capello E, Currò D, Uccelli A, Bertolotto A.... (2012) Autologous haematopoietic stem cell transplantation with an intermediate intensity conditioning regimen in multiple sclerosis: the Italian multi-centre experience. Multiple sclerosis (Houndmills, Basingstoke, England), 18(6), 835-842. PMID: 22127896  

  • April 19, 2012
  • 06:07 PM
  • 825 views

Shortcut to Success: With Induced Neural Stem Cells

by Vivek Misra in Beautiful Mind

Graphical AbstractResearchers at Universityof Bonn, Germany, have succeeded in directly generating brain stemcells from the connective tissue cells of mice. These stem cells canreproduce and be converted into various types of brain cells. Todate, only reprogramming in brain cells that were already fullydeveloped or which had only a limited ability to divide was possible.The new reprogramming method which, enables derivation of brain stemcells that are still immature and able to undergo practicallyunlimited division to be extracted from conventional body cells. Theresults have now been published in the current edition of the journalCell Stem Cell.Since Prof. ShinyaYamanaka and his team produced stem cells from the connective tissuecells of mice for the first time in 2006; these cells candifferentiate into all types of body cells. These induced pluripotentstem cells (iPS cells) develop via reprogramming into a type ofembryonic stage. This result made the scientific community sit up andtake notice. If as many stem cells as desired can be produced fromconventional body cells, this holds great potential for medicaldevelopments and drug research. Team of scientists led by Dr. FrankEdenhofer from the University of Bonn has proven a variant for thismethod in a mouse model. Study team also involved epileptologists andthe Institute of Human Genetics of the University of Bonn, led by Dr.Markus Nöthen, who is also a member of the German Center forNeurodegenerative Diseases.Edenhofer and hisco-workers Marc Thier, Philipp Wörsdörfer and Yenal B. Lakes usedconnective tissue cells from mice as a starting material. Same asProf. Yamanaka, the group initiated the conversion with a combinationof four genes. However the team deliberately target the production ofneural stem cells or brain stem cells, not pluripotent iPSmultipurpose cells. These cells are known as somatic or adult stemcells, which can develop into the cells typical of the nervoussystem, neurons, oligodendrocytes and astrocytes.The gene "Oct4"is the central control factorThe gene "Oct4"is a crucial control factor. First, it prepares the connective tissuecell for reprogramming, later, however, Oct4 appears to preventdestabilized cells from becoming brain stem cells. While this factoris switched on during reprogramming of iPS cells over a longer periodof time, the Bonn researchers activate the factor with specialtechniques for only a few days. Findings report that, this molecularswitch is toggled over a limited period of time, the brain stemcells, which the group refer as induced neural stem cells (iNScells), can be reached directly. Oct4 activates the process,destabilizes the cells and clears them for the direct reprogramming.However, further studies are required to analyze the exact mechanismof the cellular conversion.Hence, the researcherhave thus found a new way to reprogram cells, which is considerablyfaster and also safer in comparison to the iPS cells and embryonicstem cells. Since the protocol cut down on the reprogramming of thecells via the embryonic stage, the current method is about two tothree times faster than the method used to produce iPS cells by Prof.Yamanaka. Thus the work involved and the costs are also much lower.In addition, the novel Bonn method is associated with a dramaticallylower risk of tumors. As compared to other approaches, the currentmethod stands out due to the production of neural cells that can bemultiplied to a nearly unlimited degree.Low risk of tumor andunlimited self renewalA low risk of tumorformation is important because in the distant future, neural cellswill replace defective cells of the nervous system. A vision of thevarious international scientific teams is to eventually create adultstem cells for example from skin or hair root cells, differentiatethese further for therapeutic purposes, and then implant them indamaged areas. However, the scientists have a rather urgent needtoday for a simple way to obtain brain stem cells from the patient touse them to study various neurodegenerative diseases and test drugsin a Petri dish. The novel method could form the basis for providingpractically unlimited quantities of the patient's own cells. Thecurrent study was initially conducted on mice. Bonn's research teamis now looking forward to validate the findings in humans.Thier M, Wörsdörfer P, Lakes YB, Gorris R, Herms S, Opitz T, Seiferling D, Quandel T, Hoffmann P, Nöthen MM, Brüstle O, & Edenhofer F (2012). Direct conversion of fibroblasts into stably expandable neural stem cells. Cell stem cell, 10 (4), 473-9 PMID: 22445518... Read more »

Thier M, Wörsdörfer P, Lakes YB, Gorris R, Herms S, Opitz T, Seiferling D, Quandel T, Hoffmann P, Nöthen MM.... (2012) Direct conversion of fibroblasts into stably expandable neural stem cells. Cell stem cell, 10(4), 473-9. PMID: 22445518  

  • April 12, 2012
  • 05:26 AM
  • 1,062 views

Stressful Life May Leads to Alzheimer's Diseases

by Vivek Misra in Beautiful Mind

Stress can be defined as any type of change that causes physical, emotional or psychological strain. However, not all types of stress are harmful or even negative. There are a few different types of stress that we encounter viz. Eu-stress, Acute Stress, Episodic Acute Stress, Chronic Stress. Stress manifests itself in the form of many psychological and physical problems like anxiety, hopelessness, anger, helplessness, egoism, expectation, tension, constipation, irritation, depression, apathy, frustration, loss of memory, loss of mind’s balance and finally suicide. It has also been reported that people suffering from stress are more likely to be psychologically distressed than those who are not. According to a recent study published in March 26 issue of PNAS by team of researchers at University of California, San Diego School of  Medicine, repeated stress triggers the production and accumulation of insoluble tau protein aggregates inside the brain cells of mice which  may define a link between stress and an AD-related pathogenic mechanism.The aggregates are similar to neurofibrillary tangles or NFTs, modified protein structures that are one of the physiological hallmarks of Alzheimer's disease. The findings may at least partly explain why clinical studies have found a strong link between people prone to stress and development of sporadic Alzheimer's disease (AD), which accounts for up to 95 percent of all AD cases in humans.Using rodent models researcheres found that repeated episodes of emotional stress, which has been demonstrated to be comparable to what humans might experience in ordinary life, resulted in the phosphorylation and altered solubility of tau proteins in neurons, these events are critical in the development of NFT pathology in Alzheimer's disease.The effect was most notable in the hippocampus, a region of the brain linked to the formation, organization and storage of memories. In AD  patients, the hippocampus is typically the first region of the brain affected by tau pathology and the hardest-hit, with substantial cell death and shrinkage.Not all forms of stress are equally threatening. In earlier research, Rissman and colleagues reported that acute stress -- a single, passing episode -- does not result in lasting, debilitating long lasting changes in accumulation of phosphorylated tau. Acute stress-induced modifications in the cell are transient and on the whole, probably beneficial.Researchers added that, "Acute stress may be useful for brain plasticity and helping to facilitate learning. Chronic stress and continuous activation of stress pathways may lead to pathological changes in stress circuitry. As people age, perhaps their neuronal circuits becoming less robust and perhaps less capable of completely rebounding from the effects of stress. Age is the primary, known risk factor for Alzheimer's disease. It may be that as we age, our neurons just aren't as plastic as they once were and some succumb."The researchers observed that stress cues impacted two key corticotropin-releasing factor receptors, suggesting a target for potential therapies. Authors also discussed the drugs that already exist and are in human trials (for other conditions) that modulate the activity of these receptors. Although we can't just eliminate stress. We all need to be able to respond at some level to stressful stimuli. The idea is to use an antagonist molecule to reduce the effects of stress upon neurons. The stress system can still respond, but the response in the brain and hippocampus would be toned down so that it doesn't result in harmful, permanent damage.In the acknowledgement, authors dedicate this work to long time mentor and colleague, Dr. Wylie Vale, whose years of pioneering work deciphering and describing the stress system were fundamental to this paper. Vale passed away earlier this year at the age of 70.Rissman RA, Staup MA, Lee AR, Justice NJ, Rice KC, Vale W, & Sawchenko PE (2012). Corticotropin-releasing factor receptor-dependent effects of repeated stress on tau phosphorylation, solubility, and aggregation. Proceedings of the National Academy of Sciences of the United States of America PMID: 22451915... Read more »

Rissman RA, Staup MA, Lee AR, Justice NJ, Rice KC, Vale W, & Sawchenko PE. (2012) Corticotropin-releasing factor receptor-dependent effects of repeated stress on tau phosphorylation, solubility, and aggregation. Proceedings of the National Academy of Sciences of the United States of America. PMID: 22451915  

  • April 2, 2012
  • 11:01 AM
  • 890 views

Neuroscience Behind Cocktail Parties

by Vivek Misra in Beautiful Mind

photo source: forum.china.org.cnCocktail Parties, the status symbol of the modern society. Whether it is formal conference or a social get-together, cocktail parties always hold an alluring place in any event. Men holding finest liquor, standing in circles, participating in short talks, cheering-up, sharing experiences. Well, the topic of the conversation varies from philosophical opinions to variety of necktie available in a well-known store. Last weekend, I attended one such cocktail party at a defense club, which I found boring so I decided to sit on the couch with my drink and observe people. After sometime, an idea cracked into my mind, “Do our brain respond differently in Cocktail Parties?”Suppose you're at a cocktail party, and, like at most cocktail parties, there are a handful of conversations happening around the room. Have you ever wonder despite the tedious roar of laughter and dialogue, you have no trouble focusing on the voice of the person with whom you are speaking? You see her eyes and lips moving and you understand every word she is saying. But as often happens, you begin to lose interest in the conversation. Though you continue to nod your head and say things like, "Uh-huh, Oh really?" you consciously turn your attention to a hoot wit of a more tempting conversation happening elsewhere in the room.How is it that in a blink of an eye, we're able to selectively refocus our auditory attention to a distant conversation, while ignoring the conversation that's happening right in front of us? The answer, it turns out, is a mystery of our beautiful mind.According to Anthony Zador, a Professor of Biology and Program Chair of Neuroscience at the Cold Spring Harbor Laboratory, the brain mechanisms responsible for any kind of attention, whether visual or auditory, are probably not fundamentally different. However, the challenge of understanding how the brain  focus on one sound whilst ignoring the rest (a.k.a. the cocktail party problem) is twofold. With the advent of computers, scientists trying programming computers to recognize speech in controlled situations and quiet rooms as far back as ten years ago, but when deployed in real world settings with background noise their algorithms fail completely. According to Dr. Zador, the first issue with computation is: We have a whole bunch of different sounds and from a bunch of different sources and they are superimposed at the level of the ears and somehow they’re added together and to us it’s typically pretty effortless to separate out those different threads of the conversation, but actually that’s a surprisingly difficult task.The second issue is one of selection. When we listen to one conversation over another, we are choosing to redirect our auditory attention, but neuroscientists have yet to discover how the routing of these decisions happens. Now we know that the cochlea in our ears receives sound waves. Within the cochlea, there are neurons that are exquisitely sensitive to minute changes in pressure. Together, these neurons act in the cochlea as a spectral analyzer—some are sensitive to low frequency sounds, others are sensitive to middle frequency sounds and others are sensitive to high frequency sounds—and each is coded separately along a set of nerve fibers that lead to the brain's thalamus. The thalamus acts as a "modulator" for all sensory inputs, converting distinctly different input from the eyes and ears into a "standard form" before passing it to the cortex of the brain.Attention is a special case of routing sensory inputs where brain faces problem all the time, because when you attend to let’s say your sounds rather than your visual input or when you attend to one particular auditory input out of many, what you’re doing is your selecting some subset of the inputs. Elucidating the mechanism underlying attention is the basis of Zador's research.Goal of the current research is to understand how attention works in humans, but the neural activity of rodents is more easily manipulated and analyzed than that of primate monkeys or humans. To study the auditory attention of rodents, Zador's designed a special behavioral box in which his colleagues and he have trained rodents to perform attentional tasks. The setup looks like a miniature sized talk-show set, in which the participant—a rat—is asked to choose between three ports by sticking his nose through a whole. When the rat sticks his nose through the center port, he breaks an LED beam that signals a computer to deliver a specified type of stimuli, such as a high or low frequency sound. When the computer presents a low frequency sound, for example, the rat goes to one of the ports and then gets a reward, a small amount of water. If the rat breaks the beam and receives a different frequency sound, he goes to the other port and gets a reward. After a while, the rat understands what he is supposed to do and more quickly reacts to the differing frequencies. Then, the rat was challenged by masking the frequencies with low levels of white noise.Experiments demonstrate that rats can take sound stimuli and use it to guide their behavior from one port to the other. It also provides a basis to present the rats with more complicated tasks that demand the rats' attention, like manipulating when the high or low frequency is presented and how much it is masked by a distracter sounds. Group has found that when the rats ramp up their attention in expectation of hearing the sounds, the speed with which he responds to the target is faster than if the target comes unexpectedly. As one of the hallmarks of attention: an improvement in performance as measured by either speed or accuracy. Researcher also found that there are neurons in the rats' auditory cortex whose activity especially was enhanced when the rats expect to hear the target compared to when that same target is presented, but at an unexpected moment.In better understanding the neural circuits underlying attention, Zador may be paving the way for better understanding disorders like autism, which is, in large part, a disorder of neural circuits. The manifestation of the environmental and genetic causes of autism is a disruption of neural circuits and in particular, there is some reason to believe that it is a disruption of long-range neural circuits, at least in part, between the front of the brain and the back of the brain, those are the kinds of neural pathways that researchers think might be important in guiding attention. One of the ongoing projects in the lab is to examine a gene in mice that scientists think, when disrupted, cause autism in humans. Although the research is in preliminary stage, Zador is very optimistic that by understanding how autism affects these long range connections and how those long range connections in turn affect attention that we’ll gain some insight into what is going on in humans with autism. Anthony, Z. (2008). Engaging in an auditory task suppresses responses in rat auditory cortex Frontiers in Computational Neuroscience, 2 DOI: 10.3389/conf.neuro.10.2008.01.100... Read more »

Anthony, Z. (2008) Engaging in an auditory task suppresses responses in rat auditory cortex. Frontiers in Computational Neuroscience. DOI: 10.3389/conf.neuro.10.2008.01.100  

Wehr M, & Zador AM. (2003) Balanced inhibition underlies tuning and sharpens spike timing in auditory cortex. Nature, 426(6965), 442-6. PMID: 14647382  

Khalfa, S., Bruneau, N., Roge, B., Georgieff, N., Veuillet, E., Adrien, J., Barthelemy, C., & Collet, L. (2001) Peripheral auditory asymmetry in infantile autism. European Journal of Neuroscience, 13(3), 628-632. DOI: 10.1046/j.1460-9568.2001.01423.x  

Wehr M, & Zador AM. (2005) Synaptic mechanisms of forward suppression in rat auditory cortex. Neuron, 47(3), 437-45. PMID: 16055066  

  • March 22, 2012
  • 06:39 AM
  • 571 views

Genetics Analysis May Lead New Treatment for Parkinson’s Disease

by Vivek Misra in Beautiful Mind

Parkinson’s disease (PD) is a neurodegenerative disorder in which mainly nerve cells in the substantia nigra of the brain die. This region is a central area of the brain that is involved in the motor activity. The cells in this area produce a neurotransmitter that is called dopamine and why these cells specifically succumb in PD is not completely clear. The most consistent pathological finding in Parkinson’s disease is degeneration of the melanin-containing cells in the pars compacta of the substantia nigra (melanin is an inert by-product of the synthesis of dopamine). However, recent research produced hints that the dopamine-producing cells in the substantia nigra are particularly sensitive to disruptions in the energy production of the cells.Brain cells in general are very dependent on well-working energy production machinery, as their energy requirements are among the highest in the body: the brain uses about 20% of the body’s energy, while it has only about 2% of the body’s weight which might make the brain more sensitive than other organs to disruptions in this system. It has been known since a while that the cell’s power plants called mitochondria often show defects in PD patients.A study that was recently published in the journal Science Translational Medicine now shows even more conclusive evidence that energy production is impaired in this disorder. The researchers analyzed the expression of genes in tissue samples collected from diseased PD patients and found 10 different sets of genes showing decreased expression in the patients that was not found in healthy controls. Interestingly, all ten sets of genes pointed to one common activator as a master-regulator of cellular energy production, a protein called peroxisome proliferator–activated receptor g coactivator-1a (PGC-1a). It is known since longer that activation of PGC-1a can treat PD in mouse models of the disease. This decrease in action of the PGC-1a gene that ultimately leads to the demise of the dopamine producing neurons in the substantia nigra probably starts years before the appearance of the first symptoms of the disease.Still, these findings open new avenues in treating early disease and preventing further damage to the nerve cells and progression of the disorder. Medications that can activate PGC-1a are already in use for other diseases like for example diabetes. Unfortunately it is not possible to simply give these medications to PD patients, as they can only work if they can get to the brain. A biological barrier that protects our brains from toxic substances that are in the blood stream like alcohol, drugs, and toxic degradation products of the metabolism called the blood-brain-barrier also keeps these medications out of the brain. Nevertheless, the knowledge what kind of medications can activate PGC-1a can lead to a faster development of drugs that can do the same and reach the necessary areas in the brain to work for PD patients.Zheng B, Liao Z, Locascio JJ, Lesniak KA, Roderick SS, Watt ML, Eklund AC, Zhang-James Y, Kim PD, Hauser MA, Grünblatt E, Moran LB, Mandel SA, Riederer P, Miller RM, Federoff HJ, Wüllner U, Papapetropoulos S, Youdim MB, Cantuti-Castelvetri I, Young AB, Vance JM, Davis RL, Hedreen JC, Adler CH, Beach TG, Graeber MB, Middleton FA, Rochet JC, Scherzer CR, & Global PD Gene Expression (GPEX) Consortium (2010). PGC-1α, a potential therapeutic target for early intervention in Parkinson's disease. Science translational medicine, 2 (52) PMID: 20926834... Read more »

Zheng B, Liao Z, Locascio JJ, Lesniak KA, Roderick SS, Watt ML, Eklund AC, Zhang-James Y, Kim PD, Hauser MA.... (2010) PGC-1α, a potential therapeutic target for early intervention in Parkinson's disease. Science translational medicine, 2(52). PMID: 20926834  

  • March 22, 2012
  • 06:35 AM
  • 508 views

Genetics behind Schizophrenia Revealed

by Vivek Misra in Beautiful Mind

At least half of schizophrenia patients who have no family history of the disorder harbor de novomutations, according to research published online on Sunday (August 7) in Nature Genetics, suggesting genetics may play a role even when the disease is not inherited.  Specifically, researchers sequenced the exomes, or protein-coding DNA, of 53 patients with non-inherited cases of schizophrenia—meaning they had no immediate family members nor aunts, uncles, nieces, nephews or grandparents who had the disease—as well as 22 unaffected individuals and the parents of these subjects. In 27 of the schizophrenia patients, they identified 40 new mutations in 40 different genes, including one in DGCR2, a gene located in a region of chromosome 22 known to be associated with schizophrenia.Lead researcher Maria Karayiorgou of Columbia University in New York told the BBC that “The fact that the mutations are all from different genes is particularly fascinating, It suggests that many more mutations than we suspected may contribute to schizophrenia”The reason so many different genes carried new mutations likely stems from the fact that the disease is so complex and involves a variety of genetic pathways, providing a large target for mutations. This, combined with the high rate of mutations that affected protein structure and function, could explain why the disease is so common, affecting about one in every 100 people, the authors said.Xu, B., Roos, J., Dexheimer, P., Boone, B., Plummer, B., Levy, S., Gogos, J., & Karayiorgou, M. (2011). Exome sequencing supports a de novo mutational paradigm for schizophrenia Nature Genetics, 43 (9), 864-868 DOI: 10.1038/ng.902... Read more »

Xu, B., Roos, J., Dexheimer, P., Boone, B., Plummer, B., Levy, S., Gogos, J., & Karayiorgou, M. (2011) Exome sequencing supports a de novo mutational paradigm for schizophrenia. Nature Genetics, 43(9), 864-868. DOI: 10.1038/ng.902  

  • March 21, 2012
  • 02:21 AM
  • 317 views

Rett Syndrome - Immuno-Genetic Prospective

by Vivek Misra in Beautiful Mind

Rett syndrome is a devastating genetic disease in which brain development—along with communication and motor skills—regresses after about 18 months of normal development. An Immuno-Genetic Prospective... Read more »

Derecki, N., Cronk, J., Lu, Z., Xu, E., Abbott, S., Guyenet, P., & Kipnis, J. (2012) Wild-type microglia arrest pathology in a mouse model of Rett syndrome. Nature. DOI: 10.1038/nature10907  

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