Application of CRISPR and Stem-Cell Therapy in a Potential Curative Approach to Familial Alzheimer’s Disease

Alzheimer’s disease is a neurodegenerative disease that affects millions globally, yet still lacks a definitive cure. However, an emerging cure could lie within two rising technologies: Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) and stem-cell therapy. CRISPR is a gene-editing technology derived from a bacterial defense mechanism that allows scientists to edit specific genes. Stem-cell therapy is the use of stem cells (undifferentiated cells) to restore damaged tissue, and is a form of regenerative medicine. There is a focus on using these technologies specifically for Familial Alzheimer’s disease, as its genetic cause can be more clearly identified. Therefore, this article aims to understand the potential role of CRISPR and stem-cell therapy in a curative approach for Familial Alzheimer’s disease. To fully discover their use, this study compiles existing scholarly articles and clinical trials with specific inclusion and exclusion criteria, utilizing a variety of sources to account for any discrepancies. The exploratory method was utilized to define early areas of initial insight and to better gain an understanding of a relatively new and unknown subject. Through this method, it is found that the use of CRISPR and stem-cell therapy could potentially account for the genetic causes of Familial Alzheimer’s disease as well as the symptomatic effects of the disease, thereby presenting itself as a key contender in the field of curative medicine. By utilizing CRISPR for genetic alteration, and stem-cell therapy to restore the damaged neural network, it is possible to mitigate symptoms and the lasting effects of FAD, as well as correct the genetic cause of FAD. This paper advises future researchers to further their research on potential limitations, especially concerning safety issues and potential barriers. Expanding clinical trials of CRISPR on AD patients remains an important next step. This approach could result in a cure for patients with FAD, and even potential applications for general AD with symptom management as well as gene correction.