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2017 Grants - Navarro
Monitoring the Onset and Evolution of Neuronal Dysfunctions
Gemma Navarro, M.D., Ph.D.
University of Barcelona
2017 Alzheimer’s Association Research Fellowship to Promote Diversity (AARF-D)
How do abnormal proteins move between nerve cells in Alzheimer’s disease?
Alzheimer’s disease is characterized by the build-up of beta-amyloid protein into “plaques” and tau protein into “tangles” in the brain. Recent evidence suggests that abnormal tau and beta-amyloid proteins can move from one nerve cell to another, possibly contributing to the progression of brain changes associated with Alzheimer’s. As these toxic proteins move between brain regions they can damage “synapses,” the specialized structures through which nerve cells communicate with each other. Synapses are essential to memory function and are damaged early in Alzheimer’s disease. More research is needed to understand how abnormal proteins move throughout the brain and impact nerve cell function in Alzheimer’s disease.
Gemma Navarro, M.D., Ph.D. will use a novel technology called “microfluidic devices” to study how abnormal tau and beta-amyloid proteins move between nerve cells grown in laboratory dishes. Microfluidic devices allow different types of nerve cells to be grown in separate chambers, but remain physically connected through microchannels. This means scientists can expose one group of nerve cells to tau or beta-amyloid, and examine at a microscopic level, how the abnormal proteins are transported to nerve cells in the adjacent chamber. Dr. Navarro will use nerve cells from Alzheimer’s-like mice and collect them specifically from brain regions known to be important for memory. This will help shed new light on why these cells may be especially vulnerable to the spread of abnormal proteins and synapse damage. The researchers are particularly interested to see how tau and beta-amyloid may interfere with a “docking site” on synapses called the N-methyl-D-aspartate (NMDA) receptor which is important for memory function.
The results of this work will provide new information on the mechanisms that underlie the movement of abnormal proteins throughout the brain in Alzheimer’s and other neurodegenerative diseases. These studies could also identity new targets for drug treatments aimed at preventing the movement of abnormal proteins and protecting nerve cells synapses to help slow or halt disease progression.