Screening for Novel Inhibitors of Amyloid Beta Aggregation and Toxicity as Potential Drugs for Alzheimer's Disease

AD is the most common neurodegenerative disorder characterized by progressive memory impairment and cognitive deficits. The pathology of AD is still unclear; however, several studies have shown that the aggregation of the Aβ peptide in the CNS is an exclusively pathological process involved in AD. C...

Full description

Saved in:
Bibliographic Details
Published in:International journal of molecular sciences 2023-07, Vol.24 (14), p.11326
Main Authors: Sharari, Sanaa, Vaikath, Nishant N, Tsakou, Magdalini, Ghanem, Simona S, Vekrellis, Kostas
Format: Article
Language:English
Subjects:
Advertising executives
aggregation
Alzheimer's disease
amyloid beta
amyloid fibrils
Cognitive ability
Drug therapy
ginsenoside Rb1
Health aspects
Neurodegeneration
Peptides
Proteins
Ratios
salvianolic acid
Seeds
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:AD is the most common neurodegenerative disorder characterized by progressive memory impairment and cognitive deficits. The pathology of AD is still unclear; however, several studies have shown that the aggregation of the Aβ peptide in the CNS is an exclusively pathological process involved in AD. Currently, there is no proven medication to cure or prevent the disease progression. Nevertheless, various therapeutic approaches for AD show only relief of symptoms and mostly work on cognitive recovery. However, one of the promising approaches for therapeutic intervention is to use inhibitors for blocking the Aβ peptide aggregation process. Recently, herbal phenolic compounds have been shown to have a therapeutic property for treatment of AD due to their multifaceted action. In this study, we investigated the effectiveness of SA, Gn Rb1, and DMyr on inhibiting the aggregation and toxicity of Aβ40 and Aβ42 using different biochemical and cell-based assays. Our results showed that SA and DMyr inhibit Aβ40 and Aβ42 fibrillation, seeded aggregation, and toxicity. Gn Rb1 did not have any effect on the aggregation or toxicity induced by Aβ40 and Aβ42. Moreover, SA and DMyr were able to disaggregate the preformed fibrils. Overall, these compounds may be used alone or synergistically and could be considered as a lead for designing new compounds that could be used as effective treatment of AD and related disorders.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms241411326