Mitochondria Abnormalities in Alzheimers Disease

Alzheimers disease is the leading cause of dementia in the elderly. Mitochondrial dysfunction is a prominent and early feature of the disease, although the reason for this is unclear. Mitochondrial function is highly dependent on mitochondria morphology which is regulated by mitochondria fission and fusion proteins. In this study, we found disease-related changes in mitochondrial morphology and distribution as well as changes in expression levels and distribution of mitochondrial fission and fusion proteins. Interestingly, functional protein changes mimicking that found in AD, are correlated with similar changes in mitochondrial morphology and distribution to that observed in AD. We further demonstrated that ROS or amyloid-β are likely the potential pathogenic factor that causes an impaired balance of mitochondrial fission/fusion, mitochondria dysfunction and even synaptic abnormalities. Taken together, this is the first study to show that ROS or amyloid-β might induce mitochondria dynamic abnormalities in mitochondria, mitochondrial dysfunction and further neuronal dysfunction through their different effect on mitochondrial fission and fusion proteins.