TDP-43 amplifies 10 times Alzheimer ;
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beta-amyloid and tau proteins have always been considered guilty of Alzheimer’s disease. However, many people have a lot of amyloid and tau protein but not of Alzheimer’s. TDP-43 is the reason why?
Researchers have been scratching your head about this anomaly for years. TDP-43, finally, may have the answer.
Overview CBS (article and in-depth video CIAC appear below this video)
amyloid “plaques” and tau “tangles” form and increased years in the brains of people with the disease, usually before symptoms as well as memory loss become apparent.
Soon it is known about the role in memory loss and dementia of another protein, binding protein 43 kDa TAR DNA (TDP-43). TDP-43 is seen in ALS and frontotemporal dementia.
Keith Josephs, MD, Mayo Clinic, and colleagues conducted a study to determine whether TDP-43 has a independent of amyloid and tau effect, in the course and symptoms of Alzheimer’s disease. The results were reported in Conference of the International Association of Alzheimer .
The researchers conducted post-mortem examinations of the brains of 342 people who were determined to have Alzheimer’s disease based on the extent of tau tangles in the cortex. brains of subjects were examined for the presence, amount and distribution of TDP-43, and these results were correlated with the results of tests of memory and cognition taken when subjects were alive. The researchers also used MRI to evaluate atrophy in several brain regions.
InDepth-Video (article continued below the video)
After controlling for other factors, including age, amyloid deposition, genetic risk for Alzheimer’s disease and vascular disease, scientists concluded that the 195 study subjects with TDP-43 were 10 times more likely to have been cognitive decline in the death of subjects without TDP -43. They found that the “third protein” had a strong correlation with cognition, memory loss, and atrophy of the hippocampus, a brain area that is important for memory and is particularly damaged in Alzheimer’s disease.
scientists speculate that the absence of TDP-43 may help explain why some people have plaques and tangles in the brain, but do not experience dementia.
“These results show that TDP-43 amplifies loss memory and hippocampal atrophy in Alzheimer’s disease, and also appears to dominate what has been called “elastic cognition ‘in Alzheimer’s disease, where subjects remain cognitively normal despite high levels of changes in the brain Alzheimer’s, “Josephs said.” This suggests that TDP-43 is a key player in the neurodegenerative process of Alzheimer, and should be considered a potential for treating disease therapeutic target. “
TDP-43 is a key player in the clinical features associated with Alzheimer’s disease , Acta Neuropathol. June 2014, Volume 127, No. 6, pp 811-824
the Conference of the International Association of Alzheimer (CIAC) is the largest gathering of world’s leading researchers around the world focused on Alzheimer’s disease and other dementias. As part of the research program of the Alzheimer’s Association, CIAC serves as a catalyst for generating new knowledge about dementia and fostering a community of vital, collegial research. Scientists leading the advancement of research gather to report and discuss the latest data on the cause, diagnosis, treatment and prevention of Alzheimer’s disease and related disorders.
About the Alzheimer’s Association
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This article was originally published on alzheimersweekly, Read the original article here