Brief Report - (2025) Volume 9, Issue 5
Received: 01-Sep-2025, Manuscript No. jgdr-26-179192;
Editor assigned: 03-Sep-2025, Pre QC No. P-179192;
Reviewed: 17-Sep-2025, QC No. Q-179192;
Revised: 22-Sep-2025, Manuscript No. R-179192;
Published:
29-Sep-2025
, DOI: 10.37421/2684-6039.2025.09.281
Citation: Petrescu, Sofia. ”Genetics and Molecular Mechanisms of Neurodegenerative Diseases.” J Genet DNA Res 09 (2025):281.
Copyright: © 2025 Petrescu S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
The intricate molecular underpinnings of neurodegenerative diseases are at the forefront of current research, with recent advancements illuminating the genetic contributions to conditions such as Alzheimer's, Parkinson's, and Huntington's disease [1].
These investigations highlight the central roles of protein misfolding and aggregation, which lead to consequent cellular dysfunction, and explore emerging therapeutic strategies that target these molecular pathways [1].
Specifically, the genetic landscape of Parkinson's disease is being rigorously investigated, with studies identifying novel variants in key genes associated with synaptic function and protein clearance, thus providing deeper insights into disease pathogenesis [2].
The findings from such research suggest new avenues for the development of diagnostic markers and therapeutic interventions aimed at restoring neuronal health [2].
Another critical area of focus is the role of mitochondrial dysfunction in the progression of Alzheimer's disease, where specific genetic mutations have been linked to impaired energy metabolism and increased oxidative stress within neurons [3].
This work underscores the significant potential of targeting mitochondrial pathways for neuroprotection [3].
The genetic basis of Amyotrophic Lateral Sclerosis (ALS) is also being examined, with a particular emphasis on mutations in genes that regulate RNA processing and protein homeostasis [4].
This research offers crucial insights into the cellular mechanisms leading to motor neuron degeneration and points towards potential therapeutic targets for intervention [4].
Furthermore, the epigenetics of Huntington's disease is an evolving area of study, investigating how changes in gene expression, independent of DNA sequence alterations, contribute to disease onset and progression [5].
This research highlights the potential of epigenetic modifications as therapeutic targets [5].
The role of glial cells, particularly microglia and astrocytes, in the neuroinflammatory processes intrinsically linked to neurodegenerative diseases is being extensively examined [6].
Genetic factors that influence glial activation and their subsequent impact on neuronal survival are discussed, emphasizing their critical therapeutic relevance [6].
Additionally, studies are investigating the genetic predisposition to Lewy body dementia, with a focus on mutations in genes crucial for alpha-synuclein aggregation and cellular trafficking [7].
These findings contribute to a more comprehensive understanding of the molecular pathways that ultimately lead to Lewy body formation [7].
The application of advanced genomic technologies, such as whole-genome sequencing and CRISPR-based gene editing, is revolutionizing the study of neurodegenerative diseases [8].
These powerful tools are significantly accelerating the discovery of disease-associated genes and facilitating the development of novel therapeutic approaches [8].
The genetic basis of frontotemporal dementia (FTD) is another significant focus, with recent work identifying new mutations in genes that are critical for neuronal function and behavior [9].
This research lays a crucial foundation for understanding the intricate molecular pathways that drive FTD pathology [9].
Finally, the complex interplay between genetic susceptibility and environmental factors in the development of neurodegenerative diseases is being explored, with a view to understanding how gene-environment interactions can modulate disease risk and progression, offering a more holistic perspective on disease etiology [10].
Recent advancements in understanding the molecular underpinnings of neurodegenerative diseases have significantly deepened our knowledge of their genetic contributions, particularly concerning Alzheimer's, Parkinson's, and Huntington's disease [1].
These studies emphasize the critical roles of protein misfolding and aggregation, which lead to cellular dysfunction, and are actively exploring novel therapeutic strategies designed to target these specific molecular pathways [1].
In the realm of Parkinson's disease, ongoing research is meticulously investigating its genetic landscape, identifying novel genetic variants within key genes that govern synaptic function and protein clearance, thereby providing more profound insights into the underlying pathogenesis of the disease [2].
These discoveries are paving the way for the identification of new diagnostic markers and the development of targeted therapeutic interventions aimed at restoring neuronal health [2].
A crucial area of investigation revolves around the role of mitochondrial dysfunction in the progression of Alzheimer's disease, with specific genetic mutations identified as contributors to impaired energy metabolism and heightened oxidative stress within neurons [3].
This research strongly suggests the potential therapeutic benefits of interventions targeting mitochondrial pathways for neuroprotection [3].
The genetic architecture of Amyotrophic Lateral Sclerosis (ALS) is also a subject of intense scrutiny, with a particular focus on mutations in genes that play vital roles in RNA processing and protein homeostasis [4].
This research provides essential insights into the cellular mechanisms that precipitate motor neuron degeneration and highlights promising therapeutic targets for future interventions [4].
Furthermore, the field of Huntington's disease epigenetics is rapidly evolving, exploring how alterations in gene expression, independent of DNA sequence changes, contribute to the disease's onset and progression [5].
This area of study points to the considerable potential of epigenetic modifications as viable therapeutic targets [5].
The influence of glial cells, specifically microglia and astrocytes, on the neuroinflammatory processes characteristic of neurodegenerative diseases is a significant area of research [6].
Investigations into the genetic factors that modulate glial activation and their subsequent effects on neuronal survival are ongoing, underscoring their therapeutic significance [6].
Studies are also dedicated to understanding the genetic predisposition to Lewy body dementia, concentrating on mutations within genes involved in alpha-synuclein aggregation and cellular trafficking [7].
These findings are crucial for a better comprehension of the molecular mechanisms that culminate in the formation of Lewy bodies [7].
The integration of advanced genomic technologies, including whole-genome sequencing and CRISPR-based gene editing, is transforming the study of neurodegenerative diseases [8].
These cutting-edge tools are significantly accelerating the identification of disease-associated genes and are instrumental in the development of innovative therapeutic strategies [8].
The genetic basis of frontotemporal dementia (FTD) is another active area of research, with the identification of novel mutations in genes essential for neuronal function and behavior [9].
This work is fundamental to understanding the molecular pathways that drive the pathology of FTD [9].
Lastly, the complex interplay between genetic predispositions and environmental influences in the etiology of neurodegenerative diseases is being comprehensively explored [10].
This investigation emphasizes how gene-environment interactions can significantly alter disease risk and progression, offering a more comprehensive view of disease development [10].
This collection of research explores the intricate genetic and molecular mechanisms underlying major neurodegenerative diseases, including Alzheimer's, Parkinson's, Huntington's, ALS, Lewy body dementia, and frontotemporal dementia. Studies highlight the roles of protein misfolding, aggregation, mitochondrial dysfunction, and neuroinflammation, with specific attention to genetic variants and epigenetic modifications. Advanced genomic technologies are accelerating gene discovery and therapeutic development. The interplay between genetic predisposition and environmental factors is also examined, offering a comprehensive view of disease etiology and potential intervention strategies.
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