The amyloid-β peptide (Aβ) has been associated with Alzheimer’s disease (AD) for decades. The original amyloid
cascade hypothesis declared that the insoluble extracellular plaques were responsible for Aβ toxicity. Later, this hypothesis
has been updated and soluble intracellular Aβ forms and their effects within the cell have come into focus. Mitochondrial
dysfunction plays an important role in the pathophysiology of AD. Aβ was detected inside mitochondria and
several mitochondrial proteins were found to interact directly with Aβ. Such interactions can affect a protein’s function
and cause damage to the mitochondria and finally to the whole cell. This review summarizes the current knowledge of mitochondrial
proteins directly interacting with Aβ and discusses their significance for the development of therapeutics in
the treatment of AD.
Keywords: Alzheimer‘s disease (AD), amyloid-β peptide (Aβ), drug target, enzyme inhibiton, mitochondria, pharmacotherapy.
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