What is it about?
Among the pathogenetic factors of Alzheimer's disease, oxidative stress and mitochondrial dysfunction may play an essential role. Alterations of mitochondria may enhance amyloid toxicity, which in turn may aggravate mitochondrial dysfunction. We describe ultrastructural alterations of mitochondria in the soma of neurons, in axons, dendritic profiles and synaptic terminals, in astrocytes in early cases of Alzheimer’s disease on various areas of the cerebral and the cerebellar cortex, the hippocampus, the hypothalamus, the mammillary bodies and the medial geniculate body.
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Why is it important?
The morphological and morphometric study of the mitochondria revealed an impressive polymorphism at any area of the brain. The mitochondria demonstrated variation of size and shape, fragmentation of the cristae and marked changes of their structure. The most dramatic mitochondrial alterations were observed in dendritic profiles, spines and synaptic terminals. A substantial number of astrocytes demonstrated mitochondrial alterations, which coexisted with fragmentation of Golgi apparatus and dilatation of the cisternae of the smooth endoplasmic reticulum.
Perspectives
The mitochondria alterations induce a substantial decline of energy supply to neuronal processes, affecting the protein trafficking, the membrane dynamics as well as the synaptic activity, resulting in gradual synaptic and dendritic degeneration and in neuronal apoptosis eventually. Mitochondria are strategic points in the pathogenetic field of Alzheimer’s disease. New therapeutic strategies aiming at protecting the mitochondria, increasing the energy supply and preventing oxidative stress and calcium imbalance, might be beneficial in the treatment of early cases of AD.
Professor Stavros J Baloyannis or Balogiannis or Balojannis or Baloyiannis or Mpalogiannis
Aristotle University of Thessaloniki
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This page is a summary of: Mitochondria and Alzheimer’s Disease: An Electron Microscopy Study, September 2019, IntechOpen,
DOI: 10.5772/intechopen.84881.
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