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Peptides as Potential Therapeutics for Alzheimer's Disease.


ABSTRACT: Intracellular synthesis, folding, trafficking and degradation of proteins are controlled and integrated by proteostasis. The frequency of protein misfolding disorders in the human population, e.g., in Alzheimer's disease (AD), is increasing due to the aging population. AD treatment options are limited to symptomatic interventions that at best slow-down disease progression. The key biochemical change in AD is the excessive accumulation of per-se non-toxic and soluble amyloid peptides (A?(1-37/44), in the intracellular and extracellular space, that alters proteostasis and triggers A? modification (e.g., by reactive oxygen species (ROS)) into toxic intermediate, misfolded soluble A? peptides, A? dimers and A? oligomers. The toxic intermediate A? products aggregate into progressively less toxic and less soluble protofibrils, fibrils and senile plaques. This review focuses on peptides that inhibit toxic A? oligomerization, A? aggregation into fibrils, or stabilize A? peptides in non-toxic oligomers, and discusses their potential for AD treatment.

SUBMITTER: Ribaric S 

PROVIDER: S-EPMC6017258 | BioStudies | 2018-01-01T00:00:00Z

SECONDARY ACCESSION(S): NCT01689233

REPOSITORIES: biostudies

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