Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease-Reference-Cited by-同舟云学术

Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease

Published:2023-04-28 Issue: Volume: Page:105-119
ISSN:
Container-title:Exploration of Neuroprotective Therapy
language:en
Short-container-title:Explor Neuroprot Ther

Author:

Rawat Kajal¹^ORCID,Garlapally Prathiba²^ORCID

Affiliation:

1. Department of Pharmacology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India

2. CORE Regulatory, Parexel International, Hyderabad, Telangana 500081, India

Abstract

Late-onset Alzheimer’s disease (LOAD) is the most common form of Alzheimer’s disease (AD) and its risk increases exponentially with aging. The incidence of LOAD is reported to increase from 1 in every 1,000 people aged 37 to 65 in every 100 people aged 80 years and older. LOAD is extensively associated with aging and cognition decline. Several risk factors, including lifestyle choices, environmental factors, and medical ailments, affect cellular stress. The cellular stress can bring upon epigenetic alterations that affect cellular aging making the individual more susceptible to LOAD development. In due course the cellular stress resulting into epigenetic deregulation, oxidative burden, and genomic mutations leads to increased disease risk. Role of epigenetic and non-epigenetic mechanisms in accelerated cellular aging that are reported to increase the risk of LOAD development are summarized in this review. The underlying biological mechanism of cellular aging and the risk factors that could predispose cellular aging and LOAD development are also discussed in the upcoming sections.

Publisher

Open Exploration Publishing

Subject

General Medicine,Materials Chemistry,General Medicine,General Medicine,General Materials Science,General Medicine,General Medicine,Aerospace Engineering,General Medicine

Reference116 articles.

1. De-Paula VJ, Radanovic M, Diniz BS, Forlenza OV. Alzheimer’s disease. In: Harris JR, editor. Protein aggregation and fibrillogenesis in cerebral and systemic amyloid disease. Dordrecht: Springer Netherlands; 2012. pp. 329–52.

2. Ryan NS, Rossor MN. Correlating familial Alzheimer’s disease gene mutations with clinical phenotype. Biomark Med. 2010;4:99–112.

3. Alzheimer’s Association. 2019 Alzheimer’s disease facts and figures. Alzheimer’s Dementia. 2019;15:321–87.

4. Dubois B, Feldman HH, Jacova C, Hampel H, Molinuevo JL, Blennow K, et al. Advancing research diagnostic criteria for Alzheimer’s disease: the IWG-2 criteria. Lancet Neurol. 2014;13:614–29. Erratum in: Lancet Neurol. 2014;13:757.

5. Tang M, Ryman DC, McDade E, Jasielec MS, Buckles VD, Cairns NJ, et al.; Dominantly Inherited Alzheimer Network (DIAN). Neurological manifestations of autosomal dominant familial Alzheimer’s disease: a comparison of the published literature with the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS). Lancet Neurol. 2016;15:1317–25. Erratum in: Lancet Neurol. 2017;16:24.