Therapeutic implication of CRISPR gene editing in Alzheimerbs disease

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with enormous societal impact and limited curative options. The emergence of CRISPR-based genome and epigenome editing has created a new therapeutic design space: correcting pathogenic variants in autosomal-dominant AD, reprogramming major risk alleles (notably APOE), and tuning genetically implicated microglial and neuronal pathways that drive disease initiation and progression. This review synthesizes the biological rationale, summarizes CRISPR modalities most relevant to CNS therapeutics (nucleases, base editors, prime editors, CRISPRi/a, and epigenome editors), and evaluates delivery, safety, biomarker strategy, and ethical governance required for translation. We conclude with a development roadmap emphasizing target selection grounded in human genetics, CNS-optimized delivery platforms, and rigorous genomic and functional safety analytics appropriate for preventive or disease-modifying interventions. This review synthesizes the therapeutic rationale for CRISPR in AD, surveys relevant editing technologies, highlights preclinical proof-of-concept directions (including APP terminus editing and APOE editing concepts), and outlines a translational roadmap emphasizing delivery engineering, safety analytics, patient stratification, and ethical governance.