A Direct Interaction Between Mitochondrial Proteins and Amyloid-beta Peptide and its Significance for the Progression and Treatment of Alzheimer's Disease
Abstract
The amyloid-beta peptide (A beta) has been associated with Alzheimer's disease (AD) for decades. The original amyloid cascade hypothesis declared that the insoluble extracellular plaques were responsible for A beta toxicity.
Later, this hypothesis has been updated and soluble intracellular A beta forms and their effects within the cell have come into focus. Mitochondrial dysfunction plays an important role in the pathophysiology of AD.
A beta was detected inside mitochondria and several mitochondrial proteins were found to interact directly with A beta. 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 A beta and discusses their significance for the development of therapeutics in the treatment of AD.