The accumulation of β-amyloid plaques and tau protein tangles disrupts normal neuronal function, leading to synaptic dysfunction and impaired neurotransmission. As the disease progresses, neurons become increasingly vulnerable to damage and eventually undergo cell death, resulting in widespread neuronal loss, particularly in brain regions critical for memory and cognitive function, such as the hippocampus and cerebral cortex. Neuroinflammation, characterized by the activation of microglia and astrocytes, plays a significant role in the pathogenesis of AD. Chronic inflammation in the brain exacerbates neuronal damage and contributes to disease progression by releasing proinflammatory cytokines, reactive oxygen species, and other neurotoxic molecules. Vascular dysfunction and impaired cerebral blood flow are common features of AD and may contribute to neuronal damage and cognitive decline. Chronic cerebral hypoperfusion, resulting from vascular pathology, can exacerbate β-amyloid deposition and tau pathology and increase the risk of cognitive impairment. While most cases of AD are sporadic, a small percentage are inherited in an autosomal dominant fashion, known as familial Alzheimer's disease (FAD). Mutations in genes such as amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) are associated with early-onset FAD, leading to increased production or altered processing of β-amyloid. The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD) and is associated with increased β-amyloid deposition and enhanced risk of developing AD.