A Review of CRISPR Cas9 for Alzheimer’s Disease: Treatment Strategies and Could target APOE e4, APP, and PSEN-1 Gene using CRISPR cas9 Prevent the Patient from Alzheimer’s Disease? BACKGROUND: Alzheimer’s disease is a neurodegenerative disorder characterized by the formation of β-amyloid plaques and neurofibrillary tangles from hyperphosphorylated tau. Several studies suggest that targeting the deletion of the APOE e4, PSEN-1, and APP will reduce tau phosphorylation and Aβ protein accumulation, a crucial hypothesis for the causation of Alzheimer’s disease. APOE e4, PSEN-1, and APP with genome editing Clustered Regular interspersed Short Palindromic Repeats-CRISPR-related (CRISPR/Cas9) are thought to have therapeutic promise for Alzheimer’s disease.AIM: The purpose of this study was to determine whether targeting APOE e4, PSEN-1, and APP using CRISPR/Cas9 is an effective therapeutic and whether it has a long-term effect on Alzheimer’s disease.METHODS: The method used in this study summarized articles by examining the titles and abstracts of specific specified keywords. In this situation, the author picked the title and abstract that matched PubMed, Google Scholar, Science Direct, Cochrane, and the Frontiers in Neuroscience; this was followed by checking to see whether the paper was available in full-text. Eventually, the researcher will study the entire article to decide if it is valuable and relevant to the issue.RESULTS: CRISPR/Cas9 deletion of APOE e4, PSEN-1, and APP in induced pluripotent stem cells (iPSC’s) and g2576 mice as APP mutant models reduce tau phosphorylation and Aβ protein accumulation from neurofibrillary tangles and prevent cell death, vascular damage, and dementia. Furthermore, CRISPR/Cas9 deletion in APOE e4, PSEN-1, and APP improved neuronal cell resilience to oxidative stress and inflammation.CONCLUSION: APOE e4, PSEN-1, and APP deletion by genome editing CRISPR/Cas9 is effective to reduce tau phosphorylation and Aβ protein accumulation from neurofibrillary tangles, cell death, vascular damage, and dementia. However, further research is needed to determine the side effects and safety of its use.
BACKGROUND: Duchenne muscular dystrophy is a neuromuscular disease caused by a deficiency of dystrophin, which causes the skeletal and cardiac muscles to degenerate. Targeted deletion of DMD, RIPK3, and MLKL has been shown in several studies to prevent dystrophin deficiency and necroptosis, a critical hypothesis in the etiology of Duchenne muscular dystrophy. AIM: This research aimed to see if using CRISPR/Cas9 to target DMD, RIPK3, and MLKL is an effective therapeutic and if it has a long-term effect on Duchenne muscular dystrophy. METHODS: Abstracts and titles of articles were searched for specific keywords to summarize them using the method used in this study. The researcher will look over the entire article to see if it is valuable and relevant to the topic. RESULTS: CRISPR/Cas9-mediated genome editing in MDX mice can improve the primary genetic lesions that cause muscular dystrophy (DMD) and prevent disease development. Furthermore, Ripk3/Mlk1 double knockout completely blocked necroptosis susceptibility in necroptosis-sensitive cell lines, each to an indistinguishable degree. CONCLUSION: DMD, RIPK3, and MLKL gene editing by CRISPR/Cas9 is effective dystrophin insufficiency, sarcolemma fragility, poor intracellular signaling, myocyte death, inflammatory infiltration, muscle replacement, and necroptosis. However, more research is needed to determine its side effects and safety.
Background: Targeting PCSK9 by maintaining hemodynamic shear stress stability has been shown in several studies to reduce LDL-C, arterial plaque formation, and PCSK9 expression in atherosclerotic cardiovascular disease. Genome editing with CRISPR-associated regularly interspersed short palindromic repeats (CRISPR/Cas9) have therapeutic potential for atherosclerotic cardiovascular disease. This study aims to evaluate the role of CRISPR/Cas9 in targeting PCSK9 as an effective therapeutic and long-term effect on atherosclerotic vascular disease. Methods: The method used in this study summarizes the article by looking for keywords that have been determined in the title and abstract. The authors used official guidelines from Science Direct, PubMed, the American College of Cardiology, Google Scholar, and PERKI to select full-text articles published within the last decade, prioritizing searches within the last five years. Results: CRISPR/Cas9 deletion of PCSK9 in mouse models reduces LDL-C, Plaque accumulation in the arteries, and PCSK9 expression. Furthermore, CRISPR/Cas9 deletion in PCSK9 saves the stability of Hemodyanimc shear stress to control the PCSK9 expression that causes Atherosclerotic cardiovascular disease. Conclusion: PCSK9 targeting by CRISPR/Cas9 deletion effectively reduces LDL-C, plaque buildup in the arteries, and PCSK9 expression. However, more research is needed to determine its side effects and safety.
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