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2010 Grants - Asuni
Astrocytes and Synaptopathy: Protein Misfolding Disease's Mechanisms
Ayodeji Abdur-Rasheed Asuni, Ph.D.
New York University School of Medicine
New York, New York
2010 New Investigator Research Grant
Research has shown that several brain disorders, including Alzheimer's disease and the prion diseases, are instigated when misshapen proteins or protein fragments accumulate within the brain. In people at risk for Alzheimer's, build-up of the protein fragment beta-amyloid can lead to disease onset. People at risk for prion diseases show deposits of misfolded prion proteins. For all of these disorders, abnormal protein deposits often result in 1) the loss of synapses, the tiny channels through which neurons communicate with one another; and 2) an increase in the production of "helper" cells called astrocytes.
Ayodeji Abdur-Rasheed Asuni, Ph.D., and colleagues have studied mice that were engineered to develop a prion disease. They found that the animals' neurons lost cellular structures that were necessary to maintain synaptic connections. The animals also developed abnormally high levels of astrocytes and of certain proteins associated with astrocytes—proteins that were likely produced to combat damage caused by an increase in misfolded prion protein.
For this proposed grant, Dr. Asuni and colleagues will conduct a larger study with mice. Their animals will be engineered to age prematurely or to develop Alzheimer's disease or a prion disease. The researchers will assess whether deposits of misfolded beta-amyloid or prion protein lead to synaptic damage and astrocytic buildup in the mice. They will also determine whether these pathologies are associated with cognitive or behavioral problems.
The work of Dr. Asuni's team could shed new light on the role of astrocytes in multiple brain diseases. Ultimately, the study could lead to novel methods for combating such diseases at a very early stage.