Amyloid-beta peptides and their impact on Alzheimer's disease pathophysiology
Ecren Büyükada1
, Oytun Erbaş2
1Department of Molecular Biology and Genetics, Afyon Kocatepe University Faculty of Science, Afyonkarahisar, Türkiye
2Institute of Experimental Medicine, Gebze-Kocaeli, Türkiye
Keywords: Alzheimer's disease, amyloid plaque, amyloid precursor protein, neurofibrillary tangle, PSEN1, PSEN2.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with the highest incidence of dementia. Despite the accumulation of knowledge about its etiology and pathophysiology, it is still unclear. The two main pathological features of AD, hyperphosphoric Tau and insoluble amyloid-beta (Aβ) peptide, include neurofibrillary tangles and senile plaques. Genes implicated in this disorder include the amyloid precursor protein (APP), presenilin 1, and presenilin 2 genes, which are inherited in an autosomal dominant manner with early onset, as well as the apolipoprotein E gene responsible for late-onset AD. The Aβ-42, Aβ-40, and Aβ-38 proteins, which are formed as a result of proteolysis of APP to Aβ, are important biomarkers in the diagnosis and detection of AD. However, the etiology and pathology of such biomarkers need to be further investigated and characterized. This review examines the relationship between Aβ peptides and AD.
Cite this article as: Büyükada E, Erbaş O. Amyloid-beta peptides and their impact on Alzheimer's disease pathophysiology. D J Tx Sci 2023;8(1-2):35-40. doi: 10.5606/dsufnjt.2023.14
All authors contributed equally to the article.
Data Sharing Statement:
The data that support the findings of this study are available from the corresponding author upon reasonable request.
The authors declared no conflicts of interest with respect to the authorship and/ or publication of this article.
The authors received no financial support for the research and/or authorship of this article.