Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease
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 associa...
| Main Authors: | , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Open Exploration Publishing Inc.
2023-04-01
|
| Series: | Exploration of Neuroprotective Therapy |
| Subjects: | |
| Online Access: | https://www.explorationpub.com/Journals/ent/Article/100440 |
| _version_ | 1797833550406352896 |
|---|---|
| author | Kajal Rawat Prathiba Garlapally |
| author_facet | Kajal Rawat Prathiba Garlapally |
| author_sort | Kajal Rawat |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-09T14:25:25Z |
| format | Article |
| id | doaj.art-c2f13ec665904158b08ed1689786a880 |
| institution | Directory Open Access Journal |
| issn | 2769-6510 |
| language | English |
| last_indexed | 2024-04-09T14:25:25Z |
| publishDate | 2023-04-01 |
| publisher | Open Exploration Publishing Inc. |
| record_format | Article |
| series | Exploration of Neuroprotective Therapy |
| spelling | doaj.art-c2f13ec665904158b08ed1689786a8802023-05-04T07:57:00ZengOpen Exploration Publishing Inc.Exploration of Neuroprotective Therapy2769-65102023-04-013210511910.37349/ent.2023.00040Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s diseaseKajal Rawat0https://orcid.org/0000-0003-3429-840XPrathiba Garlapally1https://orcid.org/0009-0008-1343-6758Department of Pharmacology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, IndiaCORE Regulatory, Parexel International, Hyderabad, Telangana 500081, IndiaLate-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.https://www.explorationpub.com/Journals/ent/Article/100440late-onset alzheimer’s diseaseepigeneticscellular agingtelomere lengthimmunosensecence |
| spellingShingle | Kajal Rawat Prathiba Garlapally Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease Exploration of Neuroprotective Therapy late-onset alzheimer’s disease epigenetics cellular aging telomere length immunosensecence |
| title | Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease |
| title_full | Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease |
| title_fullStr | Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease |
| title_full_unstemmed | Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease |
| title_short | Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease |
| title_sort | epigenetic and non epigenetic mechanisms in the accelerated cellular aging in late onset alzheimer s disease |
| topic | late-onset alzheimer’s disease epigenetics cellular aging telomere length immunosensecence |
| url | https://www.explorationpub.com/Journals/ent/Article/100440 |
| work_keys_str_mv | AT kajalrawat epigeneticandnonepigeneticmechanismsintheacceleratedcellularaginginlateonsetalzheimersdisease AT prathibagarlapally epigeneticandnonepigeneticmechanismsintheacceleratedcellularaginginlateonsetalzheimersdisease |