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Sunday, September 19, 2010

Researchers identify genetic markers of aggressive ad

Discovered an international team of experts from the Alzheimer's disease was under the direction of Washington University School of medicine in St. Louis —, a variation of the gene predict the rate in which ad will also be progress.See: health & MedicineAlzheimer ResearchHealthy AgingDiseases and ConditionsChronic with Lewy BodiesDementiaHuntington DiseaseMenopause IllnessElder CareStroke PreventionReferenceDementia

Researchers report their findings online in the journal public library of Science (PLoS)-gene.

While previous studies have focused on the factors that influence the risk for ad, new points that determine a way to research how quickly develop complete dementia Alzheimer's patients after his diagnosis.

A protein called Tau researchers studied 846 patients with elevated privileges in the cerebrospinal fluid (CSF) .Estudios last found that the presence of a particular form the dew in CSF protein an indicator of Alzheimer Krankheit.Die researchers saw also unique DNA variations in patients and identify a genetic marker in connection with high tau.This tags that output to a rapid progression of Alzheimer's disease are associated with.

"" People institution of this genetic marker tend to higher levels of Tau have at any time the disease as individuals without it, "said senior researcher Alison M. Goate, DPhil, the Samuel and Mae S. Ludwig Professor of genetics in psychiatry.""Until now most of the risks which has genetic studies with Alzheimer's disease risk for developing the disease, not the speed with which once you have identified genetic markers as we tiene.El progression notes the progress looked."

For many patients and their families more useful than that this information may know a person can develop Alzheimer's disease, even if that person has developed clinical signs yet as Goate brain damage.Damage caused by the disease can for years, before symptoms appear.But exist that proposes this study that Tau high, combined with genetic markers could be a signal that can quickly move the clinical symptoms of mild impairment in severe dementia.

The study progress that recent research found that it possible diagnosis is Alzheimer's disease even in patients without clinical symptoms by measuring the levels of the protein beta amyloid in CSF.A beta of senile plaques in the brain of Alzheimer's patients, but it is low in the CSF A beta predict the presence of Alzheimer's disease in the brain pathology.

Meanwhile, the Tau protein accumulates to characterize the disease in the abnormal brain structures, called neurofibrilares.Los tangles cause clutter the brain cells die and Tau is released the presence of the disease when the cells die, in the Cefalorraquídeo liquid.Only low level of A beta of the CSF display associated high dew.

"Tau in stroke patients or with other types of lesions of the brain can be started," says first author Carlos Cruchaga, PhD. "but a particular form the dew specifically for Alzheimer.Es disease a form phosphorylated protein is called Ptau." "As Parkinson's disease not Ptau produce neuro-degenerative diseases high GFK.nur in Alzheimer's disease found."

Cruchaga, Assistant Professor of Psychiatry at the University of Washington, said that there was no relationship between Ptau and overall risk of Alzheimer's disease or age of onset for Alzheimer's patients, but there was a significant association between a variant of a gene, that plays a role for the change of Tau protein Ptau in the framework for community support and the rate of disease levels was promoting.

"" We examined data from three independent, international studies and three, we find the same Association, "said Cruchaga." """So, that we sure that it is real and that this variant of the gene are associated with the progression of Alzheimer's disease".

Says the genetic discovery, combined with the ability, measuring Ptau of CSF can mean if drugs that could inhibit accumulation of protein in the liquid may hinder or delay some havoc with Alzheimer's disease combined.

"If somehow we Tau could reduce Pathology at those individuals also small amounts of GfK, A beta, we the progression of the disease can slow down", says Cruchaga.

Goate said that the conclusions of first useful Clínicos.Si studies who knew in advance design researchers could be specific study patients at a pace would move faster, you could better assess the impact of drugs, designed to slow progression of Alzheimer's disease.

"" I believe that if the objective of the drug is A beta, below, must really begin treatment even before someone develops symptoms, "Goate said.""Instead, since most occurs changes in the dew if someone already has symptoms, possible this way to the progression of the disease, to slow down by interfering with the actions of Tau protein to go."



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