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2016 Grants - Forner
Impact of the Actin Cytoskeleton and its Regulators in Alzheimer’s Disease
Stefania Forner, Ph.D.
University of California, Irvine
2016 Alzheimer’s Association Research Fellowship (AARF)
How does damage to the cellular structures needed for nerve cell communication contribute to Alzheimer’s disease?
Nerve cells in the brain communicate with one another using rapid chemical signals that are transmitted through tiny channels called synapses. Information passed through synapses is received by “dendrites” which are arm-like extensions on nerve cells. In early Alzheimer’s disease, people experience damage to both synapses and dendrites — problems that may contribute to decline in memory and other cognitive functions.
In previous studies, Stefania Forner, Ph.D., and colleagues found that Alzheimer’s-like mice have alterations in the “actin cytoskeletons” of their nerve cells. The actin cytoskeleton helps support the structure of the nerve cell and is critical to the function of synapses and dendrites. More research is needed to better understand how alterations in the actin cytoskeleton may promote brain changes associated with Alzheimer’s disease.
For their current studies, Dr. Forner and her team will use nerve cells growing in laboratory dishes to determine how beta-amyloid and tau proteins affect the actin cytoskeleton. Beta-amyloid accumulates into “plaques” and tau into “tangles” — two hallmarks of Alzheimer’s disease. The researchers will also study brain tissue from people who had Alzheimer’s disease or mild cognitive impairment (MCI), a condition of subtle memory decline that may precede Alzheimer’s. They will examine how changes in the actin cytoskeleton of nerve cells relate to different stages of disease progression. They will focus specifically on brain regions associated with Alzheimer’s disease and measure the levels of genes and proteins that are involved in regulating the actin cytoskeleton.
The results of these studies could improve our understanding of how changes in nerve cell structure and function may promote the onset and progression of Alzheimer’s disease. Importantly, this work may identify new molecular targets for the development treatments for Alzheimer’s and other neurodegenerative diseases.