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2014 Grants - Ripoli
Intraneuronal Binding Partners of Amyloid-Beta Protein
Cristian Ripoli, Ph.D.
Universitá Cattolica del Sacro Cuore
2014 New Investigator Research Grant
Amyloid-beta (also known as beta-amyloid) is a protein fragment that plays an important role in Alzheimer’s disease. Beta-amyloid fragments can accumulate into clumps called amyloid plaques, a hallmark of Alzheimer’s disease. Research on the effects of beta-amyloid in the brain have primarily focused on how it impairs nerve cell function and causes nerve cell toxicity by binding to proteins on the outer surface of the cells. However, there is also evidence that beta-amyloid can accumulate inside of nerve cells.
Cristian Ripoli, Ph.D., and colleagues have been studying how the accumulation of beta-amyloid inside of nerve cells may affect cell function. They have observed that when beta-amyloid aggregates inside nerve cells, it can lead to impairments in synaptic transmission. Synaptic transmission is the process by which nerve cells communicate with one another, giving the brain many of its unique properties, including the ability to learn and remember.
Dr. Ripoli and colleagues have proposed to explore the mechanisms by which beta-amyloid can impair synaptic transmission from inside nerve cells. They will study a number of proteins important in synaptic transmission to determine which ones bind to beta-amyloid and how they are affected by that binding. These studies may reveal new insights into how beta-amyloid impacts nerve cell function and suggest novel ways to prevent or slow the progression of Alzheimer’s disease.