REVIEW article
Front. Cell. Neurosci.
Sec. Cellular Neuropathology
Volume 19 - 2025 | doi: 10.3389/fncel.2025.1681891
This article is part of the Research TopicHot Topics in Cellular Neuropathology (Volume III): Using CRISPR/Cas9 Technology for Deciphering Central Nervous System Disease TargetsView all articles
CRISPR-Cas9: Bridging the Gap Between Aging Mechanisms and Therapeutic Advances in Neurodegenerative Disorders
Provisionally accepted
- 1Ajman University, Ajman, United Arab Emirates
- 2King Khalid University, Abha, Saudi Arabia
- 3Baskirskij gosudarstvennyj medicinskij universitet, Ufa, Russia
- 4Northwestern University, Evanston, United States
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Neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, ALS, and spinocerebellar ataxia are becoming more prevalent as populations age, posing major global health challenges. Despite decades of research, effective treatments that halt or reverse these conditions remain elusive. Aging is the most significant risk factor in the development of these diseases, intertwining with molecular processes like DNA damage, mitochondrial dysfunction, and protein aggregation. Recent advances in gene-editing technologies, particularly CRISPR-Cas9, are beginning to shift the therapeutic landscape. This revolutionary tool allows for precise correction of genetic mutations associated with neurodegeneration, offering the potential for disease modification rather than symptom management alone. In this review, we explore how CRISPR-Cas9 is being leveraged to target key genes implicated in various neurodegenerative conditions and how it may overcome barriers posed by aging biology. We also examine the delivery systems and safety challenges that must be addressed before clinical application. With continued progress, CRISPR-Cas9 could mark a turning point in our ability to treat or even prevent age-related neurological decline.
Keywords: CRISPR-Cas9, gene editing, Neurodegenerative Diseases, Alzheimer's disease, Parkinson's disease, Huntington'sDisease, Amyotrophic lateral sclerosis (ALS), Aging
Received: 08 Aug 2025; Accepted: 30 Sep 2025.
Copyright: © 2025 Shamsi, Tasqeruddin, Khuzin and Zuberi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Azna Zuberi, azna.zuberi@northwestern.edu
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