The pathophysiological mechanism underlying Alzheimer's disease involves the aggregation and deposition of aberrant proteins in the brain. Specifically, the accumulation of β-amyloid (Aβ) peptides leads to the formation of extracellular plaques, while hyperphosphorylated tau protein forms intracellular neurofibrillary tangles.

 

These protein aggregates disrupt neuronal communication and cause synaptic dysfunction, ultimately leading to neuronal death. The ensuing inflammation and oxidative stress exacerbate the neurodegenerative process, resulting in the gradual and irreversible decline of cognitive function. Understanding the intricate molecular and cellular events involved in Alzheimer's disease is crucial for the development of effective treatments and interventions to alleviate its devastating effects on patients.