Alzheimer’s disease is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline and behavioral changes. It is driven by complex, interacting processes rather than a single cause.

Central to the disease are abnormal protein accumulations. Amyloid beta peptides aggregate into extracellular plaques, while tau protein inside neurons becomes hyperphosphorylated and forms tangles. These changes disrupt cell function, communication and structure. Emerging work emphasizes that the soluble, smaller aggregates of amyloid and tau may be more toxic than large, visible deposits.

Neuroinflammation is another key factor. Microglia and astrocytes, which normally support and protect neurons, can become chronically activated. Instead of clearing debris efficiently, they may release inflammatory molecules and contribute to synaptic damage. Genetic variants that affect immune function and lipid handling, such as those in APOE and other risk genes, modulate this inflammatory response and influence susceptibility.

Vascular dysfunction and metabolic changes in the brain also play important roles. Impaired blood flow, breakdown of the blood brain barrier and reduced clearance of waste products can accelerate protein buildup and neuronal stress. Mitochondrial dysfunction and disturbed energy metabolism further weaken neurons and synapses, especially in regions involved in memory.

Current treatments offer only symptomatic relief. Research is testing antibodies targeting amyloid or tau, small molecules that modify protein processing or aggregation, anti inflammatory strategies, and interventions to improve vascular and metabolic health. There is increasing emphasis on early diagnosis, before extensive damage occurs, and on combining pharmacological approaches with lifestyle measures such as physical activity, cognitive engagement and cardiovascular risk control.