Alzheimer's Disease
Alzheimer's disease is a progressive neurodegenerative disorder characterized by accumulation of amyloid plaques and tau tangles in the brain, leading to memory loss, cognitive decline, and loss of daily function.
What Alzheimer's disease is
Alzheimer's disease is a progressive neurodegenerative disorder and the most common cause of dementia, accounting for 60-80% of cases. It is defined biologically by the accumulation of two abnormal protein deposits in the brain: amyloid-beta plaques (clumps of abnormal protein fragments that accumulate between neurons) and neurofibrillary tangles made of hyperphosphorylated tau protein (twisted fibers that accumulate inside neurons).
These pathological changes begin in the brain 15-20 years before clinical symptoms appear, spreading from the entorhinal cortex and hippocampus — memory-critical regions — outward to other brain areas as the disease progresses. This preclinical period, when pathology is accumulating but cognition appears normal, is now a major focus of research aimed at early intervention.
Alzheimer's disease is distinct from normal aging, though both involve some degree of cognitive change. The pathological processes in Alzheimer's are qualitatively different from aging — not faster aging, but a distinct disease process with specific molecular mechanisms, identifiable biomarkers, and an increasingly defined treatment landscape.
Why it matters for cognitive health
Alzheimer's disease is the leading cause of dementia and one of the most significant healthcare challenges associated with population aging. Approximately 6.9 million Americans over 65 currently have Alzheimer's disease, and this number is projected to nearly double by 2060 without effective prevention strategies.
The early stages of Alzheimer's — preclinical Alzheimer's and mild cognitive impairment due to Alzheimer's — are now recognized as part of the disease continuum, before clinical dementia develops. This recognition is clinically important because emerging treatments are specifically approved for these early stages. Lecanemab and donanemab, approved in 2023 and 2024 respectively, slow decline in early Alzheimer's — but only if treatment begins before significant neurodegeneration has occurred.
Risk factors for Alzheimer's include age, family history, the APOE4 genetic variant, and a range of modifiable lifestyle factors: cardiovascular risk, sleep quality, exercise, and social and cognitive engagement. Optimizing modifiable risk factors throughout midlife is one of the most evidence-grounded strategies for reducing Alzheimer's risk.
Frequently asked questions
What is the difference between Alzheimer's disease and other dementias?
Alzheimer's disease is defined by specific biological features — amyloid plaques and tau tangles — and typically presents with episodic memory loss as the earliest symptom. Vascular dementia involves cognitive decline from blood vessel damage. Lewy body dementia involves alpha-synuclein deposits and often includes visual hallucinations and movement symptoms. Frontotemporal dementia involves personality and language changes before memory loss.
Is Alzheimer's disease genetic?
Alzheimer's has both genetic and non-genetic contributors. Late-onset Alzheimer's (the most common form, onset after 65) is influenced by many genetic variants, the most significant being APOE4, which increases risk two-to-threefold in carriers of one copy. Early-onset familial Alzheimer's (rare, onset before 65) can involve mutations in APP, PSEN1, or PSEN2 that are highly heritable. Having a family history increases risk but does not make Alzheimer's certain.
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