Alzheimer's disease (AD) is a global public health priority, affecting 44 million people worldwide and expected to triple by 2050. The disease is primarily driven by genetic and environmental factors, with the APOE gene being the single biggest risk factor. Pathologically, AD is characterized by amyloid plaques and neurofibrillary tangles, leading to neurodegeneration and cognitive decline. The amyloid hypothesis suggests that the accumulation of amyloid-beta (Aβ) is the primary pathological process, followed by tau pathology. However, the exact mechanisms linking these two processes remain unclear. Treatment options are limited, with acetyl-cholinesterase inhibitors and memantine being the main symptomatic treatments. Future prospects include disease-modifying therapies targeting amyloid or tau pathology, as well as personalized prevention strategies using genetic and biomarker data.Alzheimer's disease (AD) is a global public health priority, affecting 44 million people worldwide and expected to triple by 2050. The disease is primarily driven by genetic and environmental factors, with the APOE gene being the single biggest risk factor. Pathologically, AD is characterized by amyloid plaques and neurofibrillary tangles, leading to neurodegeneration and cognitive decline. The amyloid hypothesis suggests that the accumulation of amyloid-beta (Aβ) is the primary pathological process, followed by tau pathology. However, the exact mechanisms linking these two processes remain unclear. Treatment options are limited, with acetyl-cholinesterase inhibitors and memantine being the main symptomatic treatments. Future prospects include disease-modifying therapies targeting amyloid or tau pathology, as well as personalized prevention strategies using genetic and biomarker data.