CRISPR-based therapies for Alzheimer’s disease aim to tackle the condition at its genetic and molecular roots by editing genes linked to amyloid-beta production (e.g., APP, PSEN1, PSEN2), tau pathology (MAPT), microglial function (TREM2, CD33), and synaptic repair (BDNF, NGF). This approach offers precision and permanence, potentially preventing disease onset by correcting risk factors like APOE4 or halting amyloid/tau accumulation before irreversible brain damage. Preclinical studies, such as a 2023 Nature Neuroscience study showing reduced amyloid plaques via APP editing in mice, demonstrate promise. CRISPR’s multi-target potential, enhanced by AI for guide RNA design and off-target risk prediction, makes it a comprehensive solution. However, significant challenges include delivering CRISPR payloads across the blood–brain barrier, with nanoparticles and adeno-associated viruses (AAVs) still under optimization, and ensuring safety to avoid off-target genetic damage. Prime and base editing reduce these risks, but human trials for Alzheimer’s-specific CRISPR therapies are absent as of 2024, with preclinical work dominating. Given the typical timeline for advancing from preclinical to clinical trials (5–10 years for novel therapies), regulatory approval by 2030 is unlikely. Small-scale phase 1/2 trials for somatic brain editing (e.g., targeting APOE4 or TREM2) may begin within five years, but widespread acceptance requires proven safety and efficacy in larger trials, likely beyond 2030. The probability of CRISPR being accepted as a standard Alzheimer’s treatment by 2030 is approximately 20%, reflecting progress in early trials but significant hurdles in delivery, safety, and scalability. Neuron inflammation suppressors, such as anti-inflammatory drugs (e.g., NSAIDs like ibuprofen), biologics (e.g., anti-TNF antibodies like etanercept), or microglia-modulating agents (e.g., minocycline), target neuroinflammation, a key driver of Alzheimer’s progression. These suppressors aim to reduce pro-inflammatory cytokines (e.g., IL-1β, TNF-α) or shift microglia to a protective M2 state to enhance amyloid clearance and protect synapses. Their advantage lies in established delivery methods, as small molecules and biologics can cross the blood–brain barrier more readily than CRISPR payloads, and many are already FDA-approved for other conditions, enabling faster repurposing. Clinical trials, such as those with etanercept showing modest cognitive benefits or NSAIDs suggesting risk reduction in observational studies, provide a foundation. However, a 2020 Neurology meta-analysis highlighted inconsistent results, with NSAIDs failing in randomized trials and biologics showing limited disease modification. Chronic use risks side effects like immunosuppression, complicating long-term use in elderly patients. Despite these challenges, repurposing existing drugs or advancing new microglia-targeted agents (e.g., TREM2 agonists) could lead to approval within five years, especially for symptomatic relief or adjunctive therapy. The probability of inflammation suppressors being accepted as a standard Alzheimer’s treatment by 2030 is approximately 50%, driven by shorter development timelines and existing infrastructure, though limited by their inability to address upstream genetic or protein pathologies. Comparing the two, CRISPR offers greater long-term potential to “solve” Alzheimer’s by targeting its root causes—genetic risks and amyloid/tau pathways—potentially preventing or reversing disease progression. Its 20% probability of acceptance by 2030 reflects its transformative promise but significant technical barriers, particularly delivery and safety, which delay clinical adoption. Inflammation suppressors, with a 50% probability, are more likely to gain acceptance sooner due to established delivery, ongoing trials, and repurposing potential, but their impact is limited to slowing progression rather than curing the disease.