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Alzheimer''s 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- 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- might§induce mitochondria dynamic abnormalities in§mitochondria, mitochondrial dysfunction and further§neuronal dysfunction through their different effect§on mitochondrial fission and fusion proteins.