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Public Health Implications of Gene?environment Interactions in Parkinson?s Disease: A Functional and Epidemiological Perspective
Subject area: Science,Engineering and Technology · Area of research: Public Health
Abstract
Parkinson?s disease (PD) is a progressive neurodegenerative disorder, and we're learning that its causes are tied to a complex mix of genetic factors and environmental influences. While we know that certain genetic mutations and harmful environmental agents can contribute to PD on their own, it?s the interplay between these factors known as gene?environment (G?E) interactions that gives us a fuller picture of the disease's risk, variability, and progression This review aimed at bringing together the latest findings on the molecular mechanisms and epidemiological trends related to G?E interactions in PD, highlighting their importance for real-world applications and public health. By analyzing data from influential functional genomics studies, epidemiological meta-analyses, and population-based cohorts, significant genetic markers (like SNCA, LRRK2, and GBA), environmental neurotoxins (such as pesticides and heavy metals), and new mechanistic pathways, including mitochondrial dysfunction, epigenetic changes, and disruptions in the gut?brain connection was delved into. Insights from precision medicine, biomarker development, and community-focused prevention strategies was woven together. Research showed that environmental factors like paraquat and organophosphates can work together with genetic weaknesses especially low-activity PON1 variants and LRRK2 mutations to speed up the onset and progression of PD. Epigenetic changes and inflammation driven by gut microbiota play crucial roles in these interactions. Epidemiological studies have pinpointed specific geographical and occupational risk clusters, and meta-analyses support the idea that G?E interactions have a causal impact. However, we still have a gap in data from low- and middle-income countries. Grasping the interactions between genes and the environment in Parkinson's disease opens up vital avenues for identifying risks early, tailoring prevention strategies, and implementing policies that aim to minimize environmental hazards. To truly enhance public health outcomes, future studies should focus on comprehensive, multi-omics methods and ensure fair access to these advancements across various global communities.
Keywords
Parkinson?s disease, gene?environment interaction, public health, precision medicine, environmental neurotoxins, mitochondrial dysfunction, LRRK2, PON1, exposomics
References
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How to cite this paper
@article{1709807,
author = {Blessing Agbaza},
title = {Public Health Implications of Gene?environment Interactions in Parkinson?s Disease: A Functional and Epidemiological Perspective},
journal = {Iconic Research And Engineering Journals},
year = {2023},
volume = {7},
number = {3},
pages = {816-825},
issn = {2456-8880},
url = {https://www.irejournals.com/formatedpaper/1709807.pdf},
abstract = {Parkinson?s disease (PD) is a progressive neurodegenerative disorder, and we're learning that its causes are tied to a complex mix of genetic factors and environmental influences. While we know that certain genetic mutations and harmful environmental agents can contribute to PD on their own, it?s the interplay between these factors known as gene?environment (G?E) interactions that gives us a fuller picture of the disease's risk, variability, and progression This review aimed at bringing together the latest findings on the molecular mechanisms and epidemiological trends related to G?E interactions in PD, highlighting their importance for real-world applications and public health. By analyzing data from influential functional genomics studies, epidemiological meta-analyses, and population-based cohorts, significant genetic markers (like SNCA, LRRK2, and GBA), environmental neurotoxins (such as pesticides and heavy metals), and new mechanistic pathways, including mitochondrial dysfunction, epigenetic changes, and disruptions in the gut?brain connection was delved into. Insights from precision medicine, biomarker development, and community-focused prevention strategies was woven together. Research showed that environmental factors like paraquat and organophosphates can work together with genetic weaknesses especially low-activity PON1 variants and LRRK2 mutations to speed up the onset and progression of PD. Epigenetic changes and inflammation driven by gut microbiota play crucial roles in these interactions. Epidemiological studies have pinpointed specific geographical and occupational risk clusters, and meta-analyses support the idea that G?E interactions have a causal impact. However, we still have a gap in data from low- and middle-income countries. Grasping the interactions between genes and the environment in Parkinson's disease opens up vital avenues for identifying risks early, tailoring prevention strategies, and implementing policies that aim to minimize environmental hazards. To truly enhance public health outcomes, future studies should focus on comprehensive, multi-omics methods and ensure fair access to these advancements across various global communities.},
keywords = {Parkinson?s disease, gene?environment interaction, public health, precision medicine, environmental neurotoxins, mitochondrial dysfunction, LRRK2, PON1, exposomics},
month = {September},
}