Troy T. Rohn

Boise State University, USA 0000-0002-8406-1956

The primary focus of my laboratory is involved in the research involving neurodegenerative diseases including to a large extent, Alzheimer’s disease (AD). A primary question in this field is how are neurons dying during the progression of AD. Our lab is convinced that the primary cause of neuronal cell death associated with AD is caused by neurons undergoing apoptosis. Apoptosis, or programmed cell death, is a genetically driven form of cell suicide that plays an important function for living organisms. Upon activation of apoptosis, a series of steps occur, ultimately leading to cell death. One of the most important early steps in apoptosis is the activation of a family of proteases termed, caspases. A major role of caspases is to clip, cleave, snip and cut critical proteins in the cell, which signals the cell to commit suicide. Since neurons cannot divide, once this program is activated it is a catastrophic event for the neuron that leads to cell death. In our lab, biochemical markers are being developed that are designed to follow specific cleavage products produced from caspases. In this way, we can use these markers as footprints to the contribution of apoptosis in certain neurodegenerative diseases including AD. To do this we generate site-directed antibodies that recognize the caspase-cleaved form of proteins that may then be used in Western blot analysis and immunohistochemistry. We recently designed an antibody to caspase-cleaved beclin-1 by using the antibody, our lab discovered that in Alzheimer’s patients beclin-1 is indeed cleaved by caspases leading to its inactivation. Our data support the idea that the snipping of beclin-1 by caspases may prevent it from removing the toxic trouble-maker, beta-amyloid from the Alzheimer’s disease brain. Our lab is currently investigating the proteolytic cleavage of apoE4 and whether this cleavage is the mechanism leading to enhanced AD risk for those harboring this allele.

Biography Updated on 19 June 2012

Scholarly Contributions [Data Provided by scopus]

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