February 29, 2012

Damaging Alzheimer's Proteins Further Studied

Author Info

Reviewed by: 
Joseph V. Madia, MD By:

Article Rating

2.636365
Average: 2.6 (22 votes)
Your rating: None

Alzheimers Disease protein causes genetic blockade

(dailyRx News) There is no cure for Alzheimer’s disease, but new and advanced research provides insights that could lead to more effective treatment and early recognition of the disease.

A protein called histone deacetylase 2 (HDAC2) has been found to accumulate in the brain during the early stages Alzheimer’s in both mice and people. The good news is that in mice, clearing the accumulation of HDAC2 also prevents memory loss.

"Ask you doctor about new treatments for Alzheimer’s."

Li-Huei Tsai, Ph.D., director of The Picower Institute for Learning and Memory at the Massachusetts Institute of Technology and an investigator at the Howard Hughes Medical Institute, led the study.

A toxic protein fragment called beta-amyloid is the typical indicator of Alzheimer’s disease, and the team believes that the two are inherently linked. In fact, mouse neurons exposed to beta-amyloid produced more of the HDAC2 protein.

"We think beta-amyloid triggers a cascade of damaging reactions. Once of these is to activate HDAC2, which in turn blocks the expression of genes needed for brain plasticity," adds Tsai.

The researchers found that HDAC2 tightens up DNA, which reduces gene activity. This blockade especially effected genes involved in learning and memory. When the team prevented the buildup of HDAC2 in mice, memory loss was also prevented.

They also examined HDAC2 levels in the autopsied brains of 19 people who had Alzheimer’s at varying stages. Elevated HDAC2 was present even at the earliest stages of the disease.

"These findings provide a glimpse of the brain shutting down the ability to form new memories gene by gene in Alzheimer's disease, and offer hope that we may be able to counteract this process," said Roderick Corriveau, Ph.D., a program director at National Institutes of Health National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research.

The study was published in the journal Nature on Feb. 29th, 2012, and funded by NINDS and the National Institute on Aging. Additional support was provided through the national Institutes of Health Blueprint for Neuroscience Research and its Neuroplasticity initiative.

Share this story:

Reviewed by: 
Joseph V. Madia, MD
Review Date: 
February 28, 2012

Last Updated:
April 9, 2012