The Potential Treatment of Alzheimer’s Disease: Through CRISPR-Cas9 Genome Editing

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Named after Dr. Alois Alzheimer who discovered the disease in 1906, Alzheimer’s disease is the progressive deterioration of the brain that slowly destroys cognitive function. While some treatments exist to alleviate the symptoms of Alzheimer’s disease, there is no cure.

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Considering that researchers have studied the disease for over 100 years, making steps toward finding a cure is urgent. With evidence for the potential risk and protective factors of Alzheimer’s disease, dementia, and cognitive decline, researchers are now looking at gene editing as a solution. The CRISPR-Cas9 system, is an inexpensive, yet powerful, tool used by researchers to alter DNA sequences and gene function that has already shown promise in other neurological disorders. Through gene editing, the CRISPR-Cas9 system would go beyond the temporary lessening of Alzheimer’s disease’s symptoms and potentially prevent or stop the depreciation of the brain by targeting associated genes and correcting genetic defects. When examining the applications of CRISPR-Cas9, however, it is important to factor in both the ethical concerns of using this biotechnology, including the extent to which CRISPR should be permitted and who should have access to this technology, and concerns of not using it. While the system presents many ethical concerns and lingering questions, CRISPR-Cas9 provides a revolutionary and much-needed potential solution to Alzheimer’s disease.

In researching potential treatments for Alzheimer’s disease, it is necessary to examine both types: early onset and late onset.1 Early-onset Alzheimer’s disease, also called familial Alzheimer’s disease (FAD), occurs in people between the ages of 30 and 60 and represents less than 10% of all cases. FAD has a strong genetic component caused by mutations on chromosomes 1, 14, and 21.6 Mutations on chromosome 1 lead to the formation of amyloid precursor protein (APP), and those on 14 and 21 lead to the formation of abnormal presenilin 1 (PSEN1) and abnormal presenilin 2 (PSEN2) respectively. Late onset Alzheimer’s disease occurs in patients over the age of 60 and represents over 90% of all Alzheimer’s cases. In addition to genetic factors, lifestyle and environmental factors such heart and metabolic conditions also contribute to this type of Alzheimer’s disease. The apolipoprotein E (APOE) gene, particularly the APOE e4 allele is associated with increased risk of developing Alzheimer’s. Therefore, in order to cure Alzheimer’s disease, these genes should be targeted specifically, yet there is no guarantee this will be a solution given the impact of environmental factors.

Plaques and tangles are the two neurobiological markers of Alzheimer’s disease as opposed to dementia. Plaques are clumps of amyloid beta protein, which is derived from APP cleaved by beta secretase and gamma secretase, that breakdown brain cells by disrupting cell communication. Brain cells use an internal support and transport system that transports essential nutrients and materials. This system requires the normal structuring and function of a protein,

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