Alzheimer's disease is the leading cause of dementiain the elderly. Mitochondrial dysfunction is aprominent and early feature of the disease althoughthe reason for this is unclear. Mitochondrialfunction is highly dependent on mitochondriamorphology which is regulated by mitochondria fission and fusion proteins. In thisstudy we found disease-related changes inmitochondrial morphology and distribution as well aschanges in expression levels and distribution ofmitochondrial fission and fusion proteins.Interestingly functional protein changes mimickingthat found in AD are correlated with similar changesin mitochondrial morphology and distribution to thatobserved in AD. We further demonstrated that ROS oramyloid-? are likely the potential pathogenic factorthat causes an impaired balance of mitochondrialfission/fusion mitochondria dysfunction and evensynaptic abnormalities. Taken together this is thefirst study to show that ROS or amyloid-? mightinduce mitochondria dynamic abnormalities inmitochondria mitochondrial dysfunction and furtherneuronal dysfunction through their different effecton mitochondrial fission and fusion proteins.
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