Peptides as Potential Therapeutics for Alzheimer’s Disease
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 limit...
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doaj-d9abbf7490b74b21a08a1e61762487d12020-11-24T21:03:08ZengMDPI AGMolecules1420-30492018-01-0123228310.3390/molecules23020283molecules23020283Peptides as Potential Therapeutics for Alzheimer’s DiseaseSamo Ribarič0Institute of Pathophysiology, Faculty of Medicine, Zaloška 4, SI-1000 Ljubljana, SloveniaIntracellular 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 (Aβ(1-37/44), in the intracellular and extracellular space, that alters proteostasis and triggers Aβ modification (e.g., by reactive oxygen species (ROS)) into toxic intermediate, misfolded soluble Aβ peptides, Aβ dimers and Aβ oligomers. The toxic intermediate Aβ products aggregate into progressively less toxic and less soluble protofibrils, fibrils and senile plaques. This review focuses on peptides that inhibit toxic Aβ oligomerization, Aβ aggregation into fibrils, or stabilize Aβ peptides in non-toxic oligomers, and discusses their potential for AD treatment.http://www.mdpi.com/1420-3049/23/2/283aggregationAlzheimer’s diseaseamyloid β oligomersamyloid β peptideamyloid β plaquesinsulinneurofibrillary tanglestau proteinpeptidespeptide therapy |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Samo Ribarič |
spellingShingle |
Samo Ribarič Peptides as Potential Therapeutics for Alzheimer’s Disease Molecules aggregation Alzheimer’s disease amyloid β oligomers amyloid β peptide amyloid β plaques insulin neurofibrillary tangles tau protein peptides peptide therapy |
author_facet |
Samo Ribarič |
author_sort |
Samo Ribarič |
title |
Peptides as Potential Therapeutics for Alzheimer’s Disease |
title_short |
Peptides as Potential Therapeutics for Alzheimer’s Disease |
title_full |
Peptides as Potential Therapeutics for Alzheimer’s Disease |
title_fullStr |
Peptides as Potential Therapeutics for Alzheimer’s Disease |
title_full_unstemmed |
Peptides as Potential Therapeutics for Alzheimer’s Disease |
title_sort |
peptides as potential therapeutics for alzheimer’s disease |
publisher |
MDPI AG |
series |
Molecules |
issn |
1420-3049 |
publishDate |
2018-01-01 |
description |
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 (Aβ(1-37/44), in the intracellular and extracellular space, that alters proteostasis and triggers Aβ modification (e.g., by reactive oxygen species (ROS)) into toxic intermediate, misfolded soluble Aβ peptides, Aβ dimers and Aβ oligomers. The toxic intermediate Aβ products aggregate into progressively less toxic and less soluble protofibrils, fibrils and senile plaques. This review focuses on peptides that inhibit toxic Aβ oligomerization, Aβ aggregation into fibrils, or stabilize Aβ peptides in non-toxic oligomers, and discusses their potential for AD treatment. |
topic |
aggregation Alzheimer’s disease amyloid β oligomers amyloid β peptide amyloid β plaques insulin neurofibrillary tangles tau protein peptides peptide therapy |
url |
http://www.mdpi.com/1420-3049/23/2/283 |
work_keys_str_mv |
AT samoribaric peptidesaspotentialtherapeuticsforalzheimersdisease |
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1716774051125395456 |