Alzheimer’s disease (AD), a neurodegenerative disorder characterized by the accumulation of amyloid-beta plaques and tau tangles, shows cognitive decline. Recent genetic studies have identified over 30 variants that are resilient to AD pathology, offering new therapeutic opportunities. This review explores key protective mutations of APOE3 Christchurch, RELNCOLBOS, FN1, APP A673T, BDNF Val66Met, SORL1, CR1, TREM2, PICALM, and INPP5 D genes.These affect critical pathways, including lipid metabolism, synaptic function, tau regulation, and immune response. Potential treatments are discussed, including gene therapy and neuroprotective strategies, emphasizing a shift toward precision medicine focused on genetic resilience. By reviewing case studies and relevant literatures, the work explores the mechanisms by which these variants mitigate amyloid accumulation, tau pathology, neurodegeneration, and neuroinflammation, the key contributors to AD progression. Understanding these protective pathways offers critical insights into potential therapeutic applications, such as gene therapy, immune-modulating treatments, and personalized medicine approaches tailored to the individual’s genetic profile. The findings highlight the potential to leverage genetic protection mechanisms to develop precision interventions for AD, offering new hope to prevent or delay disease onset and progression. These discoveries could transform future treatment strategies, shifting the focus from risk management to exploiting genetic resilience to combat AD.

Alzheimer’s disease (AD), a neurodegenerative disorder characterized by the accumulation of amyloid-beta plaques and tau tangles, shows cognitive decline. Recent genetic studies have identified over 30 variants that are resilient to AD pathology, offering new therapeutic opportunities. This review explores key protective mutations of APOE3 Christchurch, RELNCOLBOS, FN1, APP A673T, BDNF Val66Met, SORL1, CR1, TREM2, PICALM, and INPP5 D genes.These affect critical pathways, including lipid metabolism, synaptic function, tau regulation, and immune response. Potential treatments are discussed, including gene therapy and neuroprotective strategies, emphasizing a shift toward precision medicine focused on genetic resilience. By reviewing case studies and relevant literatures, the work explores the mechanisms by which these variants mitigate amyloid accumulation, tau pathology, neurodegeneration, and neuroinflammation, the key contributors to AD progression. Understanding these protective pathways offers critical insights into potential therapeutic applications, such as gene therapy, immune-modulating treatments, and personalized medicine approaches tailored to the individual’s genetic profile. The findings highlight the potential to leverage genetic protection mechanisms to develop precision interventions for AD, offering new hope to prevent or delay disease onset and progression. These discoveries could transform future treatment strategies, shifting the focus from risk management to exploiting genetic resilience to combat AD.

Alzheimer’s disease (AD), a neurodegenerative disorder characterized by the accumulation of amyloid-beta plaques and tau tangles, shows cognitive decline. Recent genetic studies have identified over 30 variants that are resilient to AD pathology, offering new therapeutic opportunities. This review explores key protective mutations of APOE3 Christchurch, RELNCOLBOS, FN1, APP A673T, BDNF Val66Met, SORL1, CR1, TREM2, PICALM, and INPP5 D genes.These affect critical pathways, including lipid metabolism, synaptic function, tau regulation, and immune response. Potential treatments are discussed, including gene therapy and neuroprotective strategies, emphasizing a shift toward precision medicine focused on genetic resilience. By reviewing case studies and relevant literatures, the work explores the mechanisms by which these variants mitigate amyloid accumulation, tau pathology, neurodegeneration, and neuroinflammation, the key contributors to AD progression. Understanding these protective pathways offers critical insights into potential therapeutic applications, such as gene therapy, immune-modulating treatments, and personalized medicine approaches tailored to the individual’s genetic profile. The findings highlight the potential to leverage genetic protection mechanisms to develop precision interventions for AD, offering new hope to prevent or delay disease onset and progression. These discoveries could transform future treatment strategies, shifting the focus from risk management to exploiting genetic resilience to combat AD.

Alzheimer’s disease (AD), a neurodegenerative disorder characterized by the accumulation of amyloid-beta plaques and tau tangles, shows cognitive decline. Recent genetic studies have identified over 30 variants that are resilient to AD pathology, offering new therapeutic opportunities. This review explores key protective mutations of APOE3 Christchurch, RELNCOLBOS, FN1, APP A673T, BDNF Val66Met, SORL1, CR1, TREM2, PICALM, and INPP5 D genes.These affect critical pathways, including lipid metabolism, synaptic function, tau regulation, and immune response. Potential treatments are discussed, including gene therapy and neuroprotective strategies, emphasizing a shift toward precision medicine focused on genetic resilience. By reviewing case studies and relevant literatures, the work explores the mechanisms by which these variants mitigate amyloid accumulation, tau pathology, neurodegeneration, and neuroinflammation, the key contributors to AD progression. Understanding these protective pathways offers critical insights into potential therapeutic applications, such as gene therapy, immune-modulating treatments, and personalized medicine approaches tailored to the individual’s genetic profile. The findings highlight the potential to leverage genetic protection mechanisms to develop precision interventions for AD, offering new hope to prevent or delay disease onset and progression. These discoveries could transform future treatment strategies, shifting the focus from risk management to exploiting genetic resilience to combat AD.