What is it about?

Morphological alterations of mitochondria even in the early stages of Alzheimer’s disease underline the crucial role that mitochondrial structural changes and dysfunction play in the pathogenesis of Alzheimer’s disease and other neurodegenerative diseases, which are associated with oxidative alteration, calcium dysregulation, synaptic loss and apoptosis.

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Why is it important?

The mitochondrial dysfunction may be initiated many years prior to clinical phenomenology of Alzheimer’s disease , resulting in gradual synaptic degeneration, given that synaptic mitochondria play a crucial role in maintaining synaptic function and plasticity . It is important to underline that mitochondrial alterations are associated with synaptic loss in AD patients, even before amyloid aggregations are detected . Morphological and morphometric studies revealed that at early stages of AD the number of mitochondria in synaptic components is considerably decreased and their morphology changed substantially.

Perspectives

Therapeutic strategies targeting mitochondria may be beneficial in the initial stages of Alzheimer’s disease. Thus protection to mitochondria by inhibition of mitochondrial β-oxidation, and therapeutic application of mitochondrial enhancers and molecules supporting the Electron Transport Chain (ETC) might play a positive role in a prodromal stage of Alzheimer’s disease. In experimental level modulation of mitochondrial complex I activity proved to be beneficial in multiple animal models of familial Alzheimer’s disease . Blockade of Cyclophilin D, which is a part of the mitochondrial permeability transition pore, may enlarge the therapeutic perspectives at the initial stage of Alzheimer’s disease . Controlling mitophagy may also ameliorate the clinical phenomena in some phenotypes of Alzheimer’s disease .

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: Strategic Point in the Field of Alzheimer’s Disease, Alzheimer’s & Neurodegenerative Diseases, May 2016, Herald Scholarly Open Access,
DOI: 10.24966/and-9608/100004.
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