The pathogenesis of AD involves a complex interplay of genetic, environmental, and age-related factors, leading to progressive neurodegeneration and cognitive decline. One of the defining features of AD is the accumulation of β-amyloid protein fragments in the brain, leading to the formation of insoluble plaques. β-Amyloid is produced from the cleavage of a larger protein called amyloid precursor protein (APP) by enzymes known as β-secretase and γ-secretase. Abnormal processing of APP, along with impaired clearance of β-amyloid from the brain, results in the accumulation of β-amyloid plaques, which are toxic to neurons and disrupt synaptic function (Figure ). (B) Formation of neurofibrillary tangles by the tau protein and subsequent neuron death in tauopathies such as Alzheimer's disease. In pathologies, tau becomes hyperphosphorylated and detaches from microtubules, which causes microtubule destabilization; phosphorylated tau aggregates to form neurofibrillary tangles.