Role of Epigenetic Modulation in Neurodegenerative Diseases: Implications of Phytochemical Interventions.
Mani Iyer PrasanthBhagavathi Sundaram SivamaruthiClerance Su Yee CheongKanika VermaTewin TencomnaoJames Michael BrimsonAnchalee PrasansuklabPublished in: Antioxidants (Basel, Switzerland) (2024)
Epigenetics defines changes in cell function without involving alterations in DNA sequence. Neuroepigenetics bridges neuroscience and epigenetics by regulating gene expression in the nervous system and its impact on brain function. With the increase in research in recent years, it was observed that alterations in the gene expression did not always originate from changes in the genetic sequence, which has led to understanding the role of epigenetics in neurodegenerative diseases (NDDs) including Alzheimer's disease (AD) and Parkinson's disease (PD). Epigenetic alterations contribute to the aberrant expression of genes involved in neuroinflammation, protein aggregation, and neuronal death. Natural phytochemicals have shown promise as potential therapeutic agents against NDDs because of their antioxidant, anti-inflammatory, and neuroprotective effects in cellular and animal models. For instance, resveratrol (grapes), curcumin (turmeric), and epigallocatechin gallate (EGCG; green tea) exhibit neuroprotective effects through their influence on DNA methylation patterns, histone acetylation, and non-coding RNA expression profiles. Phytochemicals also aid in slowing disease progression, preserving neuronal function, and enhancing cognitive and motor abilities. The present review focuses on various epigenetic modifications involved in the pathology of NDDs, including AD and PD, gene expression regulation related to epigenetic alterations, and the role of specific polyphenols in influencing epigenetic modifications in AD and PD.
Keyphrases
- dna methylation
- gene expression
- genome wide
- anti inflammatory
- cerebral ischemia
- copy number
- oxidative stress
- binding protein
- traumatic brain injury
- poor prognosis
- cognitive decline
- resting state
- inflammatory response
- lipopolysaccharide induced
- blood brain barrier
- subarachnoid hemorrhage
- cell free
- brain injury
- cognitive impairment
- circulating tumor
- artificial intelligence
- long non coding rna