N. Sun, S. A. Funke and D. Willbold Pages 388 - 398 ( 11 )
Alzheimer’s disease (AD) is a devastating neurodegenerative disorder and the most common cause of dementia. Today, only palliative therapies are available. The pathological hallmarks of AD are the presence of neurofibrillary tangles and amyloid plaques, mainly composed of the amyloid-β peptide (Aβ), in the brains of the patients. Several lines of evidence suggest that the increased production and/or decreased cleavage of Aβ and subsequent accumulation of Aβ oligomers and aggregates play a fundamental role in the disease progress. Therefore, substances which bind to Aβ and influence aggregation thereof are of great interest. A wide range of Aβ binding peptides were investigated to date for therapeutic purposes. Only very few were shown to be effective in rodent AD models or in clinical studies. Here, we review those peptides and discuss their possible mechanisms of action.
Alzheimer’s disease, amyloid-β, D-enantiomer, mirror image phage display, therapeutic peptide, β-sheet breaker
Forschungszentrum Julich, ICS-6, Structural Biochemistry, Germany.