Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics.
Why it matters
In a genome-wide meta-analysis of 94,437 people with or without clinically diagnosed late-onset Alzheimer's disease, researchers confirmed 20 known genetic risk locations and found five new ones (IQCK, ACE, ADAM10, ADAMTS1 and WWOX). They also confirmed the immune-system variant HLA-DR15 as a risk factor. The genes point to immunity, lipid metabolism, tau-binding proteins and amyloid processing, and the authors say more rare variants remain to be found. These are statistical associations with risk: the study tests no treatment and does not show that any of these genes causes the disease.
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Bapineuzumab did not improve clinical outcomes in patients with Alzheimer's disease, despite treatment differences in biomarkers observed in APOE ε4 carriers.
Why it matters
In two large phase 3 trials, the anti-amyloid antibody bapineuzumab given to people with mild-to-moderate Alzheimer's disease produced no significant difference from placebo on the main measures of cognition and daily function. This means the drug did not work as hoped in these patients, and it is not a treatment for Alzheimer's disease.
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Homozygous loss-of-function mutations in TREM2, encoding the triggering receptor expressed on myeloid cells 2 protein, have previously been associated with an autosomal recessive form of early-onset dementia.
Why it matters
This genetic study sequenced the TREM2 gene in 1,092 people with Alzheimer's disease and 1,107 controls. It pooled data on one TREM2 variant, R47H, from three genome-wide studies and checked that variant in a further 1,887 cases and 4,061 controls. The summary held here describes the methods but not the results, so see the original paper for what was found. It is a genetics study and does not test any treatment, cure, or prevention.
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84/100
This study found that a commercially available plasma p-tau217 immunoassay accurately identified biological AD, comparable with results using CSF biomarkers, with reproducible cut-offs across cohorts.
Why it matters
A commercially available plasma p-tau217 immunoassay accurately identified biological Alzheimer's disease, comparable to cerebrospinal fluid biomarkers, with reproducible cut-offs across cohorts. Using a three-range reference reduced confirmatory testing by about 80%, which could make diagnosis less invasive and more accessible.
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Among persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment.
Why it matters
This analysis of many studies found that amyloid buildup in the brain becomes more common with age and is more frequent in people with mild cognitive impairment than in those with normal thinking, and that it can appear 20 to 30 years before dementia symptoms. It helps explain when amyloid pathology starts, but it does not provide a way to treat, cure or prevent Alzheimer's disease.
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ARIA is an adverse event associated with donanemab treatment that requires safety monitoring.
Why it matters
This analysis of donanemab trials found that amyloid-related imaging abnormalities (ARIA) are an adverse event associated with donanemab treatment that requires safety monitoring. Several baseline factors were linked to higher or lower risk of ARIA-E.
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Of 3285 included participants, the mean (SD) age was 70.4 (7.45) years; 1706 participants (52%) were female, 2661 (81%) had mild cognitive impairment due to Alzheimer disease, and 1777 (54%) used symptomatic medications for Alzheimer disease.
Why it matters
This report describes amyloid-related imaging abnormalities in two phase 3 studies of aducanumab in people with early Alzheimer disease. The provided text does not include information on whether aducanumab affected cognitive or functional outcomes.
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The drug did not prevent clinical progression in a trial involving patients with mild-to-moderate dementia due to Alzheimer's disease.
Why it matters
This trial tested verubecestat, a BACE-1 inhibitor that blocks production of amyloid-beta, in patients with prodromal Alzheimer's disease. The drug did not prevent clinical progression in an earlier trial involving patients with mild-to-moderate dementia due to Alzheimer's disease.
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Primary outcome was feasibility of the multimodal intervention, evaluated by recruitment rate during a 6-month recruitment phase, overall adherence in each intervention arm, and 6-month retention rate.
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Among 68 756 unique individuals, analyses included 21 852 East Asian (demographic data not available), 5738 Hispanic (68.2% female; mean [SD] age, 75.4 [8.8] years), 7145 non-Hispanic Black (hereafter referred to as Black) (70.8% female; mean [SD] age, 78.4 [8.2] years), and 34 021 non-Hispanic White (hereafter referred to as White) (59.3% female; mean [SD] age, 77.0 [9.1] years) individuals.
Why it matters
In 68,756 East Asian, Hispanic, Black and White individuals, links between APOE genotype and Alzheimer disease differed by ancestry: the ε2 genotypes (ε2/ε2, ε2/ε3) showed no association with AD in East Asian people (OR 0.97), and Hispanic people showed weaker APOE associations that overall ancestry could not explain. A previously reported higher risk for women with the ε3/ε4 genotype was seen again in White individuals, but at ages 60 to 70 (OR 1.48), and also in a combined analysis of Black and Hispanic individuals (OR 1.72). These are statistical associations; they do not give anyone a personal risk figure and do not point to a treatment.
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82/100
Tau accumulation in patients with Alzheimer's disease tracks closely with cognitive decline and plays a role in the later stages of disease progression.
Why it matters
This phase 2 randomized, double-blind, placebo-controlled trial tested the anti-tau antibody tilavonemab at three doses against placebo in patients with early Alzheimer's disease over 96 weeks. The available text does not report whether tilavonemab affected the primary endpoint.
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In TRAILBLAZER-ALZ, 272 participants (mean [SD] age, 75.2 [5.5] years; 145 [53.3%] female) were randomized.
Why it matters
In this exploratory secondary analysis of the TRAILBLAZER-ALZ randomized trial, which randomized 272 people with early symptomatic Alzheimer disease, blood levels of pTau217 and glial fibrillary acidic protein were significantly lower with donanemab than with placebo "as early as 12 weeks after the start of treatment", and those changes were correlated with the percent change in amyloid. Blood amyloid-β 42/40 and neurofilament light chain showed "no significant differences" between arms at the end of treatment. This record reports blood-marker changes only: it does not say whether memory or daily function changed, and it is not evidence that the treatment cures or prevents Alzheimer's disease.
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Alzheimer's disease is a progressive, irreversible, and fatal disease for which accumulation of amyloid beta is thought to play a key role in pathogenesis.
Why it matters
EMERGE and ENGAGE were two randomized, double-blind, placebo-controlled phase 3 trials of aducanumab, an antibody against clumped forms of amyloid beta, in people with early Alzheimer's disease, run at 348 sites in 20 countries. The authors set out to evaluate the drug's "efficacy and safety", but the text held here describes only the design and aims and reports no results, so this page cannot tell you whether aducanumab helped or what side effects it caused. Read the original paper for the findings.
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Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate Alzheimer's disease and was associated with treatment-related adverse events.
Why it matters
This randomized trial found that verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate Alzheimer's disease and was associated with treatment-related adverse events. It shows no benefit from this drug for treating the disease.
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Alzheimer's disease is characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles.
Why it matters
This double-blind, placebo-controlled phase 3 trial tested the humanized monoclonal antibody solanezumab, designed to increase clearance of soluble Aβ from the brain, in patients with mild dementia due to Alzheimer's disease. Participants had MMSE scores of 20 to 26 and amyloid deposition shown by florbetapir positron-emission tomography or Aβ1-42 measurements in cerebrospinal fluid.
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The likelihood of amyloid positivity was associated with age and APOE ε4 status.
Why it matters
Amyloid plaques also occur in other dementias, so this meta-analysis pooled individual data on 1,359 people clinically diagnosed with Alzheimer's dementia and 538 with other dementias, and found that a positive amyloid PET scan was associated with diagnosis, age and APOE ε4 status. In Alzheimer's dementia the estimated share with a positive scan fell from 86% at age 50 to 68% at 90 in APOE ε4 non-carriers, and from 97% to 90% in carriers. The authors see potential use in telling dementias apart in early-onset cases and in supporting an Alzheimer's diagnosis in non-carriers over 70; the study is about diagnosis, not treatment.
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Among patients with probable Alzheimer disease and agitation who were receiving psychosocial intervention, the addition of citalopram compared with placebo significantly reduced agitation and caregiver distress; however, cognitive and cardiac adverse effects of citalopram may limit its practical application at the dosage of 30 mg per day.
Why it matters
In a double-blind trial of 186 people with probable Alzheimer disease and agitation, all already receiving psychosocial support, 40% of those given citalopram showed moderate or marked improvement versus 26% on placebo, and caregiver distress also fell. It did not improve the NPI agitation subscale or daily activities, and the authors warn that cognitive and cardiac side effects "may limit its practical application" at 30 mg per day.
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The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3).
Why it matters
In a three-stage genome-wide study by the Alzheimer Disease Genetics Consortium, common variants at MS4A4A, CD2AP, EPHA1 and CD33 were associated with late-onset Alzheimer's disease after checks in two further replication stages (for example, MS4A4A across all three stages: P = 8.2 × 10⁻¹²). The study also confirmed earlier links at CR1, CLU, BIN1 and PICALM, but not at EXOC3L2. The record reports how unlikely each signal is to be chance, not how much any variant changes risk, so it cannot predict an individual's risk and it tested no treatment.
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This 2026 update is an even larger follow-up to the 2022 Bellenguez GWAS, combining data from nearly 1 million people.
Why it matters
This 2026 update is an even larger follow-up to the 2022 Bellenguez GWAS, combining data from nearly 1 million people, and brought the total number of Alzheimer's-linked genetic regions to 91 (16 newly found). It showed that people in the highest tenth of a genetic risk score were roughly twice as likely to show severe tau tangle and amyloid plaque pathology when their brains were examined after death.
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EVOKE (ClinicalTrials.gov NCT04777396) and EVOKE+ (NCT04777409) tested whether oral semaglutide, the GLP-1 diabetes/weight-loss drug, could slow early Alzheimer's disease progression in a combined 3,808 participants over up to 156 weeks.
Why it matters
In two Phase 3 trials of 3,808 participants, oral semaglutide showed no significant difference from placebo in clinical decline on the main measure, and Novo Nordisk ended its Alzheimer's program for the drug after this result. Some biomarker reductions did not translate into any detectable slowing of cognitive or functional decline.
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Enrollment was undertaken between May 18, 2021, and September 8, 2023.
Why it matters
This paper sets out the design of evoke and evoke+, two large randomized, double-blind, placebo-controlled phase 3 trials of once-daily oral semaglutide versus placebo in people with early-stage symptomatic Alzheimer's disease. The trials enrolled participants between May 18, 2021, and September 8, 2023, to test efficacy, safety and tolerability. It is a design paper: it does not report whether semaglutide helped, so it should not be read as evidence that the drug works.
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Among persons with early Alzheimer's disease, the use of gantenerumab led to a lower amyloid plaque burden than placebo at 116 weeks but was not associated with slower clinical decline.
Why it matters
In two phase 3 trials, gantenerumab lowered amyloid plaque burden more than placebo at 116 weeks but was not associated with slower clinical decline. This means the drug did not slow the clinical course of early Alzheimer's disease.
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There were 813 participants in CREAD (mean [SD] age, 70.7 [8.2] years; 483 female and 330 male) and 806 in CREAD2 (mean [SD] age, 70.9 [7.7] years; 456 female and 350 male).
Why it matters
These two phase 3 trials of crenezumab in early Alzheimer's disease reported no new safety signals, with amyloid-related imaging abnormalities with edema being rare, mild, and transient. The provided text does not report efficacy results.
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BAN2401-G000-201 did not meet the 12-month primary endpoint.
Why it matters
This phase 2b trial tested lecanemab, an antibody targeting soluble aggregated amyloid beta, in people with early Alzheimer's disease, mild cognitive impairment due to Alzheimer's disease, and mild Alzheimer's disease dementia, using a Bayesian design to find the effective dose. It is a proof-of-concept trial and does not establish that lecanemab cures or prevents Alzheimer's disease.
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Alzheimer's disease (AD) is a public health priority for the 21st century.
Why it matters
This genome-wide association study identified three new Alzheimer's disease-associated loci containing genes relevant for Alzheimer's disease and neurodegeneration, and reported that the association of SNPs in TOMM40 with Alzheimer's disease is potentially mediated by gene expression and DNA methylation. It states these loci may help elucidate biological mechanisms and warrant further exploration for potential precision medicine applications, so the work is preliminary and reports no treatment or cure.