Alzheimer's disease
Atomic claims
Alzheimer's disease (AD) is a progressive neurodegenerative disease.
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Alzheimer's disease is the most common cause of dementia.
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Alzheimer's disease is defined pathologically by extracellular amyloid-β plaques.
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Alzheimer's disease is defined pathologically by intracellular tau neurofibrillary tangles.
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There is no cure for Alzheimer's disease.
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Treatment for Alzheimer's disease consists of symptomatic drugs.
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Since 2023, Alzheimer's disease treatment includes anti-amyloid antibodies.
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Anti-amyloid antibodies modestly slow decline in early Alzheimer's disease.
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Alzheimer's disease accounts for an estimated 60–70% of dementia cases.
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More than 57 million people live with dementia worldwide.
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There are nearly 10 million new diagnoses of dementia a year worldwide.
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An estimated 7.4 million Americans aged 65 and older are living with Alzheimer's disease.
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US care costs for Alzheimer's and other dementias are estimated at $409 billion in 2026.
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Alois Alzheimer described the first case of Alzheimer's disease in 1906.
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Amyloid-β was isolated as the plaque protein in Alzheimer's disease in 1984.
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Age is the strongest risk factor for Alzheimer's disease.
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Rare autosomal-dominant early-onset Alzheimer's disease is caused by mutations in the APP gene.
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The WHO attributes up to 45% of dementia risk to modifiable factors.
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Modifiable factors for dementia risk include tobacco, alcohol, inactivity, air pollution, hypertension and diabetes.
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Symptomatic drugs for Alzheimer's disease include the cholinesterase inhibitors donepezil, rivastigmine, and galantamine.
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The FDA approved lecanemab in 2023.
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In the Clarity AD trial, lecanemab slowed decline on the CDR-SB scale by about 27% over 18 months.
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In the Clarity AD trial, the 27% slower decline corresponds to a 0.45-point difference on the 18-point CDR-SB scale.
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Both lecanemab and donanemab carry a risk of amyloid-related imaging abnormalities (ARIA).
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Amyloid-related imaging abnormalities (ARIA) include brain edema or microhemorrhage.
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The lecanemab boxed warning recommends APOE ε4 testing before starting treatment.
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The EMA's CHMP recommended authorizing lecanemab in November 2024.
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The EMA's CHMP had previously issued a negative vote regarding lecanemab in July 2024.
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On May 16, 2025, the FDA approved the first blood test (Lumipulse G pTau217/Aβ1-42 ratio) to detect amyloid plaques in symptomatic patients.
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Sources disagree on whether the minimum age for the Lumipulse G pTau217/Aβ1-42 ratio blood test is 50 or 55.
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A second blood test, Roche's Elecsys pTau181, has been cleared.
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The Lumipulse test is not intended for screening.
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Amyloid accumulation precedes Alzheimer's symptoms by years.
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Antibody-driven amyloid plaque removal produces statistically significant slowing of Alzheimer's decline.
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It is contested whether amyloid is the primary cause of Alzheimer's disease or one contributor alongside tau, inflammation and vascular factors.
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Many earlier anti-amyloid trials failed.
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It is contested whether the benefit of anti-amyloid antibodies is noticeable to patients.
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Regulators and health-technology bodies have reached different conclusions regarding the clinical meaningfulness of anti-amyloid antibodies.
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The FDA granted accelerated approval to aducanumab in 2021.
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The manufacturer discontinued aducanumab in 2024.
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The 2024 Alzheimer's Association criteria define Alzheimer's disease by biomarkers.
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Critics, including the International Working Group, argue that Alzheimer's diagnosis should require clinical symptoms.
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A 2006 Nature paper on the Aβ*56 oligomer was retracted in 2024.
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How much the retraction of the 2006 Nature paper on the Aβ*56 oligomer affected the wider field is disputed.
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Alzheimer's disease is primarily characterized by the accumulation of specific misfolded proteins in the brain.
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The accumulation of misfolded proteins in Alzheimer's disease leads to the eventual impairment of basic physiological functions.
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Modern medical interventions for Alzheimer's disease encompass symptom-management medications.
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Modern medical interventions for Alzheimer's disease encompass disease-modifying therapies targeting specific neuropathological proteins.
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Alois Alzheimer observed the characteristic plaques and tangles in the brain of a deceased patient.
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A hallmark neuropathological feature of Alzheimer's disease is extracellular senile plaques composed of beta-amyloid peptides.
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A hallmark neuropathological feature of Alzheimer's disease is intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein.
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The most significant known genetic risk factor for the late-onset form of Alzheimer's disease is the presence of the ε4 allele of the Apolipoprotein E (APOE) gene.
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Early-onset familial Alzheimer's disease typically presents before age 65.
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Early-onset familial Alzheimer's disease accounts for less than 5% of all Alzheimer's cases.
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The clinical presentation of Alzheimer's disease typically begins with short-term memory impairment.
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The clinical presentation of Alzheimer's disease typically progresses to include language difficulties (aphasia).
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Standard symptomatic treatments for Alzheimer's disease include the NMDA receptor antagonist memantine.
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Acetylcholinesterase inhibitors and memantine can temporarily stabilize cognitive symptoms.
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Acetylcholinesterase inhibitors and memantine do not halt the underlying neurodegeneration of Alzheimer's disease.
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In 2023, the U.S. Food and Drug Administration (FDA) granted traditional approval to lecanemab.
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Lecanemab and donanemab are monoclonal antibodies designed to clear beta-amyloid plaques from the brain.
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Lecanemab and donanemab are designed to slow the rate of clinical decline.
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Diagnosis of Alzheimer's disease traditionally relied on clinical history and cognitive testing.
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Modern diagnostic criteria for Alzheimer's disease increasingly utilize biomarkers from positron emission tomography (PET) imaging to confirm the presence of amyloid and tau pathology.
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For over three decades, the dominant theoretical model for Alzheimer's disease has been the amyloid cascade hypothesis.
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The amyloid cascade hypothesis posits that the accumulation of beta-amyloid is the primary, initiating driver of the disease's pathology.
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The amyloid cascade hypothesis is contested by a subset of neuroscientists and researchers.
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Critics of the amyloid cascade hypothesis argue that amyloid plaques may be a late-stage byproduct.
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Critics of the amyloid cascade hypothesis argue that amyloid plaques may be only one component of a broader multi-factor pathology that includes neuroinflammation, vascular issues, or metabolic dysfunction.
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Critics frequently point to the historical failure of numerous anti-amyloid drugs in clinical trials as evidence against the amyloid cascade hypothesis.
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The recent regulatory approvals of anti-amyloid monoclonal antibodies (such as aducanumab, lecanemab, and donanemab) have generated significant debate regarding their clinical value.
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Anti-amyloid monoclonal antibodies effectively remove amyloid plaques.
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Anti-amyloid monoclonal antibodies show a statistically significant slowing of cognitive decline in trials.
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Critics argue that the absolute slowing of decline caused by anti-amyloid monoclonal antibodies is modest.
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Anti-amyloid monoclonal antibodies carry known risks of Amyloid-Related Imaging Abnormalities (ARIA).
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There are ongoing disputes over the risk-to-benefit ratio of anti-amyloid monoclonal antibodies.
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External references: Wikidata Q11081