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Research Grants 2017

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

2017 Grants - Reid

The Consequences of Activity-Induced DNA Breaks in Alzheimer's Disease

Dylan Reid, Ph.D.
The Salk Institute for Biological Studies
La Jolla, California

2017 Alzheimer’s Association Research Fellowship (AARF)

Does DNA damage in nerve cells contribute to brain changes associated with Alzheimer’s disease?

A major focus of Alzheimer’s research is determining what genetic factors may increase the risk for disease. Evidence suggests that accumulation of damage to an individual’s DNA (genetic code) may increase risk for developing Alzheimer’s. Recent findings have shown that nerve cells must create tiny breaks in their DNA in order to activate certain genes involved in learning and memory. Normally these DNA breaks are then repaired by the DNA damage response (DDR) system, but during aging and neurodegenerative disease, declines in this repair process can lead to cumulative DNA damage. More research is needed to understand DNA breakage and repair mechanisms in nerve cells and determine if alterations in this system may contribute to Alzheimer’s disease.

Research Plan
Dylan Reid, Ph.D., will use a novel imaging method called super-resolution microscopy (SRM) to study how DNA breaks are repaired in nerve cells growing in laboratory dishes. SRM allows scientists to visualize DNA at a microscopic level that was not previously possible. Dr. Reid will use SRM to examine how DNA breaks are repaired by the DDR system and determine if beta-amyloid interferes with this process. Beta-amyloid is a protein fragment that forms “plaques” in the Alzheimer’s brain. The researchers will use “induced pluripotent stem cells” (iPSCs) – a special type of stem cell made from the skin cells of adults and then “reprogrammed” to become nerve cells. iPSCs allow scientists to study human nerve cells from both young and old individuals with different genetic backgrounds. They will expose the iPSCs to beta-amyloid and measure DNA breaks and the ability of the DDR to repair the damage. They hypothesize the cumulative DNA damage due to aging and exposure to beta-amyloid will impair the activity of genes related to nerve cell health and function.

The results of these studies could shed new light on the involvement of DNA damage and repair mechanisms in Alzheimer’s disease and other dementias. Preventing DNA damage or promoting its repair could offer new avenues for the development of therapies that could slow or halt Alzheimer’s disease.

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

Abstract Submissions Now Open

The Scientific Program Committee is now accepting submissions for poster
presentations, oral presentations and featured research sessions.