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[beta](1-37/44), in the intracellular and extracellular space, that alters proteostasis and triggers A[beta] modification (e.g., by reactive oxygen species (ROS)) into toxic intermediate, misfolded soluble A[beta] peptides, A[beta] dimers and A[beta] oligomers. The toxic intermediate A[beta] products aggregate into progressively less toxic and less soluble protofibrils, fibrils and senile plaques. This review focuses on peptides that inhibit toxic A[beta] oligomerization, A[beta] aggregation into fibrils, or stabilize A[beta] peptides in non-toxic oligomers, and discusses their potential for AD treatment

Keywords

Alzheimer's disease;amyloid [beta] oligomers;amyloid [beta] peptide;

Data

Language:	English
Year of publishing:	2018
Typology:	1.02 - Review Article
Organization:	UL MF - Faculty of Medicine
UDC:	616.8
COBISS:	33689817
ISSN:	1420-3049
Views:	209
Downloads:	72
Average score:	0 (0 votes)
Metadata:

Other data

Secondary language:	Slovenian
Secondary keywords:	Alzheimerjeva bolezen;amiloidni [beta] oligomeri;amiloidni peptid;
Type (COBISS):	Article
Pages:	str. [1]-31
Volume:	ǂVol. ǂ23
Issue:	ǂno. ǂ2
Chronology:	Jan. 2018
DOI:	10.3390/molecules23020283
ID:	13641453