Filamentous bacterial viruses break down amyloid plaques in an animal model of Alzheimer's disease - A novel therapeutic avenue

The current dominant theory of Alzheimer's disease (AD) etiology and pathogenesis is related to the amyloid cascade hypothesis which states that overproduction of amyloid-beta-peptide (AβP), or failure to clear this peptide, leads to Alzheimer's disease primarily through amyloid deposition, presumed to be involved in neurofibrillary tangles formation [1], Amyloid-β (Aβ) plaque formation, one of the main hallmarks of Alzheimer's disease, is a complex kinetic and thermodynamic process [2]. The dependence of AβP polymerization on peptide-peptide interactions to form a β- pleated sheet fibril, and the stimulatory influence of other proteins on the reaction suggest that amyloid formation can be modulated. Here we describe recent data on the use of filamentous phage as a delivery vector of anti-AβP antibodies which interfere with amyloid plaque formation [3], as well as novel therapeutics for disaggregation of amyloid plaques, towards a better alternative to existing attempts to treat AD.