Alzheimer’s disease is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and behavioral changes. It is associated with the abnormal buildup of two key proteins in the brain: beta amyloid, which forms plaques between neurons, and tau, which forms tangles inside nerve cells. These changes disrupt communication between neurons, trigger inflammation, and eventually cause cell death and brain shrinkage, particularly in regions involved in memory and thinking.

Current research has highlighted that Alzheimer’s likely begins years or even decades before symptoms appear. During this silent phase, amyloid plaques and tau tangles slowly accumulate while subtle changes in brain activity and structure develop. Genetics plays an important role, particularly variants of the APOE gene, which can increase susceptibility. Age remains the strongest risk factor, but cardiovascular health, metabolic disorders, head trauma, sleep disturbances, and lifestyle factors also influence risk.

Diagnosis is shifting from symptom based criteria to biological definitions supported by imaging and fluid biomarkers. Brain scans can detect amyloid and changes in brain volume, while cerebrospinal fluid and blood tests can measure amyloid, tau, and markers of neurodegeneration and inflammation.

Treatment approaches are moving beyond symptomatic relief toward disease modification. Some antibody based therapies are designed to clear amyloid from the brain, while others target tau, neuroinflammation, or metabolic pathways. Researchers are also testing combinations of drugs, lifestyle interventions such as exercise and cognitive training, and early intervention in at risk individuals. Despite setbacks and ongoing debate about the centrality of amyloid, the field is rapidly evolving toward earlier detection and more personalized therapeutic strategies.