Introducing the Role of Genotoxicity in Neurodegenerative Diseases and Neuropsychiatric Disorders

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(13), P. 7221 - 7221

Published: June 29, 2024

Decades of research have identified genetic and environmental factors involved in age-related neurodegenerative diseases and, to a lesser extent, neuropsychiatric disorders. Genomic instability, i.e., the loss genome integrity, is common feature among both (mayo-trophic lateral sclerosis, Parkinson's disease, Alzheimer's disease) psychiatric (schizophrenia, autism, bipolar depression) instability associated with accumulation persistent DNA damage activation response (DDR) pathways, as well pathologic neuronal cell or senescence. Typically, DDR signaling ensures that genomic proteomic homeostasis are maintained dividing cells, including neural progenitors, post-mitotic neurons. However, dysregulation these protective responses, part due aging insults, contributes progressive development and/or In this Special Issue, we introduce highlight overlap between disorders, emerging clinical, genomic, molecular evidence for contributions aberrant repair. Our goal illuminate importance subject uncover possible treatment prevention strategies relevant devastating brain diseases.

Language: Английский

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Effect of Aflatoxin B1 on the Nervous System: A Systematic Review and Network Analysis Highlighting Alzheimer’s Disease

Biology, Journal Year: 2025, Volume and Issue: 14(4), P. 436 - 436

Published: April 17, 2025

Exposure to aflatoxin (AF) triggers the production of inflammatory molecules and free radicals, leading chronic inflammation, cancer, neurodegenerative diseases. This systematic review evaluated effects AFB1 on nervous system, particularly focusing Alzheimer’s disease (AD). A comprehensive search was conducted in Scopus, Cochrane Library, PubMed, Web Science databases up 1 June 2024, without restrictions. From 993 records retrieved, 16 articles were included review. participates various biochemical processes pathological conditions. The study highlights that contributes AD by inducing DNA damage, oxidative stress, endoplasmic reticulum (ER) impairing repair mechanisms. results neuronal cognitive decline, neurodegeneration. also affects key signaling pathways, reduces sodium–potassium pump activity, disrupts cell cycle regulation involving p53, neurotoxicity, formation amyloid-beta (Aβ) plaques neurofibrillary tangles. Additionally, network analysis revealed 309 genes associated with AD, angiopathy, B1 (AFB1). Among these, ESR1 exhibited highest number direct connections other nodes within network. gene TP53 played a pivotal role mediating communication among genes, while EP300 significantly influenced overall structure. KEGG enrichment demonstrated these are substantially involved pathways related FoxO pathway, apoptosis, AD. In summary, causes damage decline It damages neurons, repair, contributing neurotoxicity inflammation. PROSPERO registration number: CRD420250651007.

Language: Английский

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Aflatoxin B1 exposure exacerbates chemokine receptor expression in the BTBR T+ Itpr3tf/J Mouse Model, unveiling insights into autism spectrum disorder: A focus on brain and spleen

Reproductive Toxicology, Journal Year: 2024, Volume and Issue: 126, P. 108599 - 108599

Published: April 26, 2024

Language: Английский

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Aflatoxin B1 exposure deteriorates immune abnormalities in a BTBR T+ Itpr3tf/J mouse model of autism by increasing inflammatory mediators' production in CD19-expressing cells

Journal of Neuroimmunology, Journal Year: 2024, Volume and Issue: 391, P. 578365 - 578365

Published: May 6, 2024

Language: Английский

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Contamination of the traditional medicine Radix Dipsaci with aflatoxin B1 impairs hippocampal neurogenesis and cognitive function in a mouse model of osteoporosis

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 283, P. 116831 - 116831

Published: Aug. 15, 2024

Language: Английский

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