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Research Grants 2015


To view an abstract, select an author from the vertical list on the left.

2015 Grants - Stoehr

Characterization of Naturally Occurring Alzheimer’s Disease Strains

Jan Stoehr, Ph.D.
University of California, San Francisco
San Francisco, California

2015 New Investigator Research Grant

Can the structure of beta-amyloid plaques and tau tangles determine whether or not they promote Alzheimer’s disease and other dementias?

Background
Two molecules in the brain, the protein fragment beta-amyloid and an abnormal form of tau protein, have long been thought to play significant roles in Alzheimer’s disease. These molecules tend to accumulate into clumps (known as amyloid plaques and tau tangles) that may promote the dysfunction and death of nerve cells, but the exact mechanisms underlying amyloid and tau toxicity have not been determined.

In recent years, studies have found that certain structural alterations of beta-amyloid and tau molecules promote their abnormal accumulation into protein clumps. Research has also found that some people with extensive plaque and tangle formation do not develop the clinical symptoms of Alzheimer’s disease. Taken together, these findings suggest that various forms or “strains” of beta-amyloid and tau may develop structurally distinct clumps in different individuals. Certain clumps may have a structure that promotes Alzheimer’s disease, while other clumps do not.

Research Plan
For this grant, Jan Stoehr, Ph.D., and colleagues will compare the structure of amyloid plaques and tau tangles in two types of individuals: those who have Alzheimer’s disease and those who have high levels of amyloid and tau accumulation in their brains but no dementia. They will look for key structural factors in the protein clumps that may be linked to disease-related losses in brain function. They will also examine whether tau and amyloid molecules accumulate differently in the two participant groups; and whether genetic factors can be linked to these differences.

Impact
The results of this effort could identify specific forms of amyloid and tau clumping that promote dementia onset and progression — as well as forms that do not promote disease. Such efforts could lead to novel methods of diagnosing dementia. They could also lead to new dementia therapies that could block the formation of disease-related plaques and tangles.


Alzheimer's Association International Conference | July 16-20, 2017, London, England

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