# CRISPR-Cas9: bridging the gap between aging mechanisms and therapeutic advances in neurodegenerative disorders

**Authors:** Anas Shamsi, Mohammed Alrouji, Othman AlOmeir, Syed Tasqeruddin, Khuzin Dinislam, Azna Zuberi

PMC · DOI: 10.3389/fncel.2025.1681891 · Frontiers in Cellular Neuroscience · 2025-10-16

## TL;DR

CRISPR-Cas9 gene editing may offer new ways to treat age-related neurodegenerative diseases like Alzheimer’s and Parkinson’s.

## Contribution

This review highlights novel applications of CRISPR-Cas9 in targeting genetic causes of neurodegeneration and aging-related challenges.

## Key findings

- CRISPR-Cas9 enables precise correction of genetic mutations linked to neurodegenerative diseases.
- The technology has potential to modify disease progression rather than just manage symptoms.
- Delivery systems and safety remain key challenges for clinical use.

## Abstract

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.

## Linked entities

- **Diseases:** ALS (MONDO:0004976), spinocerebellar ataxia (MONDO:0000437)

## Full-text entities

- **Diseases:** mitochondrial dysfunction (MESH:D028361), Neurodegenerative diseases (MESH:D019636), Huntington's (MESH:D006816), spinocerebellar ataxia (MESH:D020754), ALS (MESH:D008113), Alzheimer's (MESH:D000544), Parkinson's (MESH:D010300), neurological decline (MESH:D009461)

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12571817/full.md

## References

158 references — full list in the complete paper: https://tomesphere.com/paper/PMC12571817/full.md

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Source: https://tomesphere.com/paper/PMC12571817