The Inverse Relationship Between Cancer and Alzheimer's Disease: Shared Pathways, Drug Repurposing, and Novel Therapeutic Targets

There have been many statistical correlations found between cancer patients and individuals diagnosed with Alzheimer's disease (AD), where cancer survivors have shown a decrease in their risk to develop AD by 35-51% relative to other individuals of the same age (Braithwaite et al., 2025; Catalá-López et al., 2014). Nonetheless, the biological reasoning for such an outcome remains unknown and hasn’t been applied clinically in developing drugs for AD patients. Therefore, cross-domain drug repurposing has become a highly important task within the scientific community due to the relatively low efficacy of existing methods. In this systematic review, peer-reviewed evidence will be presented based on four key analysis pillars: epidemiology, molecular biology, drug repurposing, and survival bias. The evidence consists of 60 papers published during the period from 2000 to 2025 and selected by searching the PubMed database. Across the molecular biology pillar, the most common mechanistic finding was on shared dysregulation of p53 tumour suppressor activity, epidermal growth factor receptor (EGFR) signaling, and epigenetic modifications which include DNA methylation and histone acetylation. These findings operate in an opposing direction in cancer compared to AD neurons. Evidence suggests that both the inherent biology of cancer and the therapy received by patients could have mechanisms underlying the neuroprotection seen, even though survival bias contributes to approximately 40% of the inverse association. This insinuates a clear biological effect remains. This review highlights knowledge gaps which include a lack of longitudinal evidence, inadequate stratification by gender, and inadequate research on the preclinical phase of AD.