Intrinsic ability to brain learning discovered emphasis (science daily)

PharmaLive.com (13 December 2010) - medical researchers have discovered a missing link which explains the interaction between the State of the brain and triggers neurons responsible for learning, potentially open new ways to stimulate cognitive function in the face of diseases like Alzheimer's as well as strengthen memory in healthy people.

Much is known processes neurons which occur in learning so far was not clear why it occurs in some States of the brain, but not others. Now researchers at the University of Bristol were able to study specific neurotransmitter that promotes learning and memory in isolation.

Acetylcholine is released into the brain to learning and is essential for the acquisition of new memories. Its role is to facilitate the activity of NMDA, protein receptors that control the strength of the connections between nerve cells in the brain.

Currently, the only effective treatment for the symptoms of cognitive impairment seen in diseases like Alzheimer's disease is through the use of drugs that increase the amount of the release of acetylcholine and thereby improve cognitive functions.

Describing their findings in the journal Neuron, Physiology and pharmacology of Bristol school researchers demonstrated acetylcholine facilitates NMDA receptors by inhibiting the activity of others channels SK whose normal role is to limit the activity of the NMDA receptor proteins.

This Discovery Channel SK role provides new insights into the mechanisms underlying learning and memory. SK channels normally act as an obstacle to the function of the NMDA receptor, preventing changes in resistance of the connections between nerve cells and therefore limit the ability of the brain to encode souvenirs. This most recent search results show that canal SK barrier can be removed by the release of acetylcholine in the brain to enhance our ability to learn and recall information.

Principal investigator, Dr. Jack Mellor, Faculty of medicine at the University of Bristol, said: "these findings will not revolutionize the treatment of Alzheimer's disease or other forms of cognitive impairment from one day to the next." However, national and international funding agencies have recently been aging and dementia research a priority so we expect many progress more in our understanding of the mechanisms underlying learning and memory in health and disease. »

The team studied the effects of drugs that target acetylcholine receptors and SK channels on the resistance of the connections between nerve cells in the animal brain tissue. They found that changes in the strength of connection was facilitated by the presence of drugs which activate acetylcholine receptors or block channels SK revealing the relationship between the two proteins.

Dr. Mellor said: "therapeutic point of view, this study suggests that certain medications that affect specific acetylcholine receptors can be very attractive as potential treatments for cognitive disorders." Currently, only effective treatments for patients with Alzheimer's disease are drugs that boost the effectiveness of the naturally released acetylcholine. We have shown that mimic the effect of the acetylcholine to specific receptors that facilitates change in resistance of the connections between nerve cells. This could potentially be beneficial for patients with schizophrenia and Alzheimer's disease. »

CRM Center of the University of Bristol in synaptic plasticity and Division of neurosciences in the school of Physiology involved research team & Pharmacology, part of the Bristol neuroscience network. This work was supported by the Wellcome Trust, CRM, BBSRC and GSK.

Warning: this article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those PharmaLive.com or its staff.

Source of the story:

The story above is reproduced (with drafting adaptations by staff at PharmaLive.com) materials provided by University of Bristol.

Reference of the review:

Buchanan KA, Petrovic MM, SEL de Chamberlain, M. NV & Mellor. facilitation of M1 muscarinic receptor long-term potentiation is mediated inhibition of SK channels. Neuron, DOI: 10.1016/j.neuron.2010.11.018

Note: If no author is given, the source is cited for this.

Gene that causes sometimes lateral sclerosis als family discovered (science daily)

PharmaLive.com (9 December 2010) - using a new method of sequencing of the genes, a team of researchers led by scientists at Johns Hopkins and the National Institutes of Health has discovered a gene that seems to cause some cases unrelated amyotrophic lateral sclerosis (ALS). The findings could lead to new ways to treat the most common form of this fatal neurodegenerative disease that kills the vast majority of Americans close to 6,000 diagnosed with ALS each year.

Researchers don't know exactly what causes ALS, which destroys the motor neurons that control the movement of the muscles of the body, including those that control breathing. However, studies of familial disease, which affects the 5-10% of people with Alzheimer's, might shed some light on why motor neurons die in all types of ALS, says Bryan j. Traynor, M.D., Assistant Professor in the Department of Neurology at the Johns Hopkins University School of Medicine and Chief of the research group study neuromuscular diseases at the National Institutes of Health.

"If you look at the spectrum of diseases caused by the dysfunctional genes, our understanding of almost all from a familial disease," explains Traynor. By finding the genes associated with these diseases, he said, researchers can insert causative genes in animals, creation of models that can help them to decipher what's happening to cause pathologies and find ways to stop them.

Scientists were already aware of a handful of genes which seems to cause some family als cases. The new study, published in the journal Neuron, December 9 Traynor and his colleagues used a new technique called exome sequencing to seek more. This new technique differs from most common gene sequencing type because it focuses only on 1-2% of that code for proteins and ignores other non-codage DNA genome. Exome sequencing of thousands of genes at the same time, rather than sequencing step by step the more traditional method, exome sequencing much faster sequences.

The Traynor team worked with two affected members of an Italian family discovered by colleague Adriano Chiò, M.D., of the University of Turin, SLA expert who maintains a register of all cases of the disease by Jessica Mandrioli, MD, University of Modena and Italy North. Using sequencing exome on these two ALS patients and 200 people without the disease, scientists examined the differences in gene ALS patients had in common that differ from the other samples. Their research led to a gene called CRS, abbreviation of valosin containing protein.

When researchers have sought other cases in which this gene was transferred in additional 210 ALS patients, they found four different mutations affecting the VCP in five persons. None of these mutations were found in the genomes of hundreds of healthy controls, suggesting that the secure channel is indeed the cause of some of the ALS cases.

Although scientists don't always know exactly how to posted SC could lead to the SLA, they know that this gene plays a role in a process called ubiquination, the tags of proteins for degradation. A glitch in the process could result in too or too little of certain proteins are present in engines, neurons leading to death. Finally, said scientific Traynor may be able to develop drugs that could transform this pathological process a healthy patients with ALS, save the motor neurons that otherwise dead.

This work was funded in part by the NIH, National Institute on aging and the national Institute on neurological diseases and stroke intramural programming. Work was also funded by the Packard Center for research at Johns Hopkins University, the Fondazione Vialli e Mauro ALS research Onlus, Federazione Italiana Calcio unfinished, Ministero della Salute, the Muscular Dystrophy Association and the Woodruff Health Sciences Center of Emory SLA.

Jeffrey Rothstein, M.D., of Johns Hopkins University, participated in this study.

Warning: this article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those PharmaLive.com or its staff.

Source of the story:

The story above is reproduced (with drafting adaptations by staff at PharmaLive.com) materials provided by Johns Hopkins Medical Institutions.

Reference of the review:

Janel o. Johnson et al. Exome sequencing shows that CRS mutation as a cause of ALS family. Neuron, vol. 68, no. 5, 857-864, 9 December 2010 DOI: 10.1016/j.neuron.2010.11.036

Note: If no author is given, the source is cited for this.