Redox Homeostasis, Gut Microbiota, and Epigenetics in Neurodegenerative Diseases: A Systematic Review

Antioxidants, Journal Year: 2024, Volume and Issue: 13(9), P. 1062 - 1062

Published: Aug. 30, 2024

Neurodegenerative diseases encompass a spectrum of disorders marked by the progressive degeneration structure and function nervous system. These conditions, including Parkinson's disease (PD), Alzheimer's (AD), Huntington's (HD), Amyotrophic lateral sclerosis (ALS), Multiple (MS), often lead to severe cognitive motor deficits. A critical component neurodegenerative pathologies is imbalance between pro-oxidant antioxidant mechanisms, culminating in oxidative stress. The brain's high oxygen consumption lipid-rich environment make it particularly vulnerable damage. Pro-oxidants such as reactive nitrogen species (RNS) (ROS) are continuously generated during normal metabolism, counteracted enzymatic non-enzymatic defenses. In diseases, this balance disrupted, leading neuronal This systematic review explores roles stress, gut microbiota, epigenetic modifications aiming elucidate interplay these factors identify potential therapeutic strategies. We conducted comprehensive search articles published 2024 across major databases, focusing on studies examining relationships redox homeostasis, changes neurodegeneration. total 161 were included, comprising clinical trials, observational studies, experimental research. Our findings reveal that stress plays central role pathogenesis with microbiota composition significantly influencing balance. Specific bacterial taxa markers identified modulators suggesting novel avenues for intervention. Moreover, recent evidence from human animal supports emerging concept targeting homeostasis through therapies. Future research should focus validating targets settings exploring personalized medicine strategies based individual profiles.

Language: Английский

From Environment to Gene Expression: Epigenetic Methylations and One-Carbon Metabolism in Amyotrophic Lateral Sclerosis

Cells, Journal Year: 2024, Volume and Issue: 13(11), P. 967 - 967

Published: June 3, 2024

The etiology of the neurodegenerative disease amyotrophic lateral sclerosis (ALS) is complex and considered multifactorial. majority ALS cases are sporadic, but familial also exist. Estimates heritability range from 8% to 61%, indicating that additional factors beyond genetics likely contribute ALS. Numerous environmental considered, which may add up synergize throughout an individual's lifetime building its unique exposome. One level integration between genetic epigenetics, results in alterations gene expression without modification genome sequence. Methylation reactions, targeting DNA or histones, represent a large proportion epigenetic regulations strongly depend on availability methyl donors provided by ubiquitous one-carbon (1C) metabolism. Thus, understanding interplay exposome, 1C metabolism, modifications will elucidating mechanisms underlying altered related developing targeted therapeutic interventions. Here, we review evidence for metabolism methylation dysregulations ALS, with focus impairments reported neural tissues, discuss these environmentally driven as consequences cumulative exposome late hits, possible result early developmental defects.

Language: Английский

hPSCs-derived brain organoids for disease modeling, toxicity testing and drug evaluation

Experimental Neurology, Journal Year: 2024, Volume and Issue: 385, P. 115110 - 115110

Published: Dec. 10, 2024

Language: Английский