Jacob Chang
ABSTRACT
Alzheimer's disease (AD), a neurodegenerative disease, is a result of abnormal buildups of protein, such as amyloid and neurofibrillary tangles, in the brain, creating memory loss. While Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) normally functions to facilitate the removal of amyloid plaques and neurofibrillary tangles, mutations in TREM2 render it dysfunctional. Specific mutations in genes such as TREM2 have shown to be a big risk factor in AD. Gene therapy, a relatively recent discovery, can help to replace defective or missing genes. Recent advancements in gene therapy, a treatment for diseases, offer a promising avenue for treating AD by addressing defective or missing genes, such as those related to TREM2. One of the notable gene therapy systems is Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR). Here, we review CRISPR and our understanding of TREM2 in hopes of finding a potential therapeutic for AD.
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