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Mitochondria may underlie oxidative stress in Alzheimer disease (AD) changes since dysfunction is a prominent
and early feature of AD. Recent studies demonstrate that mitochondria are dynamic organelles that undergo
continual fission and fusion events which regulate their morphology and distribution. Morphometry showed a
small but significant reduction in mitochondria number and enlarged size in AD. Levels of the fission/fusion
proteins DLP1, OPA1, Mfn1 and Mfn2C were significantly decreased in AD, yet levels of Fis1 were significantly
increased. Interestingly, although all these proteins demonstrate even distribution in the cytoplasm and processes
of pyramidal neurons in age-matched control hippocampus, they appeared to accumulate in the soma but not in
the processes of pyramidal neurons in AD hippocampus. Given that OPA1, Fis1, and Mfn1/2 are all mitochondrial
membrane proteins, the changes in their distribution to soma in AD neurons, suggest changes in mitochondria
distribution in these neurons. The expression of fission/fusion proteins was manipulated in M17 cells and primary
hippocampal neurons in a way that mimicked their expression changes in AD. These manipulations all reduced
mitochondrial density in the cell periphery (M17 cells) or neuronal processes (primary neurons) which correlated
with reduced spine numbers (primary neurons). A尾PP and A尾 caused reduced expression of DLP1 and OPA1
while increasing expression of Fis1, consistent with our findings in AD brains. Through time lapse study, we
were able to demonstrate that mitochondria were able to fuse with each other but at a much slower rate in A尾PP
overexpressing cells. Overall, we concluded that A尾PP, through amyloid-尾 production impairs mitochondrial
fission/fusion balance through regulation of expression of mitochondria fission and fusion proteins.
Biography
George Perry is dean of the College of Sciences and professor of biology at The University of Texas at San Antonio, and adjunct
professor of Pathology and Neurosciences at Case Western Reserve University. Perry is recognized in the field of Alzheimer锟絪 disease
research particularly for his work on oxidative metabolism. He is distinguished as one of the top Alzheimer锟絪 disease researchers
with over 1000 publications, and one of the top 100 most-cited scientists in neuroscience and behavior. Perry is editor-in-chief for the
Journal of Alzheimer's Disease, a Fellow of the American Association for the Advancement of Sciences, the Microscopy Society of
America, the Royal Society of Chemistry, and past president of the American Association of neuropathologists, as well as a member of
the Dana Alliance for Brain Initiatives and a Fulbright Senior Specialist. Perry's research is primarily focused on how Alzheimer disease
develops and the physiological consequences of the disease at a cellular level.
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