Protein Interactome of Amyloid-beta as a Therapeutic Target

The amyloid concept of Alzheimer's disease (AD) assumes the beta-amyloid peptide (A beta) as the main pathogenic factor, which injures neural and other brain cells, causing their malfunction and death. Although A beta has been documented to exert its cytotoxic effect in a solitary manner, there is much evidence to claim that its toxicity can be modulated by other proteins. The list of such A beta co-factors or interactors includes tau, APOE, transthyretin, and others. These molecules interact with the peptide and affect the ability of A beta to form oligomers or aggregates, modulating its toxicity. Thus, the list of potential substances able to reduce the harmful effects of the peptide should include ones that can prevent the pathogenic interactions by specifically binding A beta and/or its partners. In the present review, we discuss the data on A beta-based complexes in AD pathogenesis and on the compounds directly targeting A beta or the destructors of its complexes with other polypeptides.