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2017 Grants - Masurkar
Lateral Entorhinal Cortex-CA1 Interactions in Alzheimer’s Disease
Arjun Masurkar, M.D., Ph.D.
New York University School of Medicine
New York, New York
2017 Alzheimer’s Association Clinical Fellowship (AACF)
Why are specific brain regions involved in memory vulnerable to the toxic effects of beta-amyloid?
Nerve cells in the brain communicate with each other via tiny specialized structures called synapses which are essential for memory function. One of the earliest brain changes associated with Alzheimer’s disease is the loss of these important synapses. Evidence suggests that when beta-amyloid accumulates in the brain during Alzheimer’s disease it can damage synapses. It is not yet understood why certain types of nerve cells are more vulnerable than others to the toxic effects of the beta-amyloid protein.
Arjun Masurkar, M.D., Ph.D. and colleagues will study how beta-amyloid oligomers inside nerve cells lead to loss of synapses and disruption in nerve cell communication. Oligomers are small, abnormal clumps of beta-amyloid that are thought to be particularly toxic to nerve cells in the early stages of Alzheimer’s disease. The researchers will focus their efforts on synapses between two brain regions important for learning and memory — the lateral entorhinal cortex and hippocampal CA1 region. The researchers will measure changes in synaptic function and the activity of nerve cell pathways between these regions in Alzheimer’s-like mice. They aim to identify the specific nerve cells most vulnerable to the toxic beta-amyloid oligomers.
These studies could improve our understanding of the earliest effects of beta-amyloid on nerve cell function in Alzheimer’s disease. The results of this work could also identify new avenues for the development of therapies that protect vulnerable nerve cells and help slow or halt the progression of Alzheimer’s disease.