Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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In participants with prodromal to mild AD in this randomized clinical trial, semorinemab did not slow clinical AD progression compared with placebo throughout the 73-week study period but did demonstrate an acceptable and well-tolerated safety profile.
Why it matters
In this phase 2 trial, semorinemab did not show a difference from placebo on the primary outcome measure of clinical dementia rating. Similar increases on the Clinical Dementia Rating-Sum of Boxes score were seen in the placebo and semorinemab groups.
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Both t-tau and p-tau are suitable AD blood biomarkers, and p-tau217 is more sensitive than other tau biomarkers to differentiate MCI and AD.
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The variability in disease onset was compared with that of autosomal dominant Alzheimer disease.
Why it matters
In this meta-analysis of people with Down syndrome, Alzheimer disease began at an estimated 53.8 years on average and death followed at about 58.4 years, roughly 4.6 years after onset. US death records showed the typical age at death rising from 1 year in 1968 to 57 in 2019, but the oldest deaths (90th percentile) barely moved, from 63 to 65 years. The authors say this ceiling and the consistent age at onset are "compatible with fully penetrant Alzheimer disease". The study describes the course of the disease and does not test any treatment or prevention.
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In addition, several loci associated with rare variants, including a genome-wide significant intergenic locus near IGF1R at 15q26 (P = 1.7 × 10-9) and 6 additional loci with suggestive significance (P ≤ 5 × 10-7) such as API5 at 11p12 (P = 8.8 × 10-8) and RBFOX1 at 16p13 (P = 5.4 × 10-7) were identified.
Why it matters
African American people are about twice as likely as their non-Hispanic White neighbours to develop Alzheimer's, so this study looked for genetic risk signals in 2,784 African American people with Alzheimer's and 5,222 without it. It found one genome-wide significant region near the IGF1R gene and 6 weaker "suggestive" regions. Of 25 risk regions known from non-Hispanic White studies, only 7 (APOE, ABCA7, TREM2, BIN1, CD2AP, FERMT2 and WWOX) were implicated in this group. These are statistical associations, not proven causes, and the study tested no treatment or prevention.
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Concentrations of plasma p-tau181 were compared with established CSF and PET biomarkers and longitudinal measurements using Spearman correlation, area under the curve (AUC), and linear regression analyses.
Why it matters
This study, using data from four prospective cohorts, tested how well a blood measure of phosphorylated tau 181 (p-tau181) matched established spinal-fluid (CSF) and PET brain-scan markers of Alzheimer's disease, and whether it could be used in prediction models of change over time. Our record holds only the study's methods, not its results, so it cannot tell you how accurate the blood test was — check the original paper before drawing any conclusion. It evaluates a diagnostic test and does not test any treatment, cure or prevention.
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Among 2218 AMARANTH patients, the mean (SD) age was 71.3 (7.1) years, and 1177 of 2218 (53.1%) were women.
Why it matters
These trials were designed to assess whether lanabecestat slows progression of early and mild Alzheimer's disease compared with placebo. The provided text does not report the efficacy results.
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Our study confirmed the effectiveness of psychosocial interventions for improving cognition or slowing down the progression of cognitive impairment in AD patients and recommended several interventions for clinical practice.
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Dose group efficacy required a significant benefit over placebo for the primary end point and 1 or more key secondary end points.
Why it matters
In three large trials, idalopirdine added to cholinesterase inhibitors did not improve cognition compared with placebo over 24 weeks. This means idalopirdine is not supported as a treatment for mild to moderate Alzheimer disease.
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The study was stopped early for futility, but dose-dependent effects observed in exploratory analyses on select clinical and biomarker endpoints suggest that higher dosing with gantenerumab may be necessary to achieve clinical efficacy.
Why it matters
In this 2-year phase III trial (SCarlet RoAD), 797 people with prodromal Alzheimer's disease were randomized to monthly injections of gantenerumab 105 mg, 225 mg or placebo. The trial was stopped early for futility, with no difference from placebo on the main measure of decline (CDR-SB) or on secondary clinical measures. Brain-scan changes called ARIA, mostly without symptoms, became more common with higher dose and in APOE ε4 carriers; the authors' suggestion that higher doses might be needed comes from exploratory analyses only.
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Genome-wide significance in fully adjusted models (sex, age, APOE genotype, population stratification) was observed for a SNP in ABCA7 (rs115550680, allele = G; frequency, 0.09 cases and 0.06 controls; odds ratio [OR], 1.79 [95% CI, 1.47-2.12]; P = 2.2 × 10(-9)), which is in linkage disequilibrium with SNPs previously associated with Alzheimer disease in Europeans (0.8 Conclusions and relevance In this meta-analysis of data from African American participants, Alzheimer disease was significantly associated with variants in ABCA7 and with other genes that have been associated with Alzheimer disease in individuals of European ancestry.
Why it matters
This meta-analysis in African Americans found a genome-wide significant link between a variant in the ABCA7 gene and late-onset Alzheimer's disease. Identifying such variants may help point to targets for genetic testing, prevention, and treatment.
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Two loci were identified to have genome-wide significance for the first time: rs744373 near BIN1 (odds ratio [OR],1.13; 95% confidence interval [CI],1.06-1.21 per copy of the minor allele; P = 1.59x10(-11)) and rs597668 near EXOC3L2/BLOC1S3/MARK4 (OR, 1.18; 95% CI, 1.07-1.29; P = 6.45x10(-9)).
Why it matters
Combining genome-wide scans of more than 35,000 people (8,371 with Alzheimer's), this study found two gene regions, near BIN1 and near EXOC3L2/BLOC1S3/MARK4, linked to Alzheimer's at genome-wide significance for the first time, each adding modest odds (1.13 and 1.18 per copy of the variant), and confirmed them, along with CLU and PICALM, in a separate Spanish sample. The authors state these loci 'did not improve AD risk prediction' and are 'not clinically useful', though they 'may implicate biological pathways useful for future research.'
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Trial registration clinicaltrials.gov Identifier: NCT00056225.
Why it matters
This trial tested high-dose folate, vitamin B6, and vitamin B12 supplementation in 409 individuals with mild to moderate Alzheimer disease and normal levels of these vitamins and homocysteine. The provided text does not report whether the supplements affected cognitive decline.
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Tacrine, the first of the cholinesterase inhibitors to undergo extensive trials for this purpose, was associated with significant adverse effects including hepatotoxicity.
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Using cross-population GWAS meta-analyses, we identify novel LOAD susceptibility loci in/near LRRC4C and LHX5-AS1, both with known roles in neuronal development, as well as several novel population-unique loci.
Why it matters
Pooling genetic data from 56,241 people of White, African American, Hispanic and East Asian ancestry, this study found 13 gene regions linked to late-onset Alzheimer's across populations, including two new ones near LRRC4C and LHX5-AS1, plus population-specific regions near PTPRK, GRB14 and KIAA0825. The authors say including diverse ancestries boosts the power to find risk genes, which can point to new biological pathways to study.
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Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous.
Why it matters
Using cerebrospinal fluid proteomics in 3,397 individuals, the ratio YWHAG:NPTX2 explained variance in cognitive impairment beyond amyloid-beta and tau measures and predicted conversion from cognitively normal to mild cognitive impairment and from mild cognitive impairment to dementia. It is described as a prognostic biomarker, not a treatment, cure, or prevention.
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These results show that in addition to APOE ε4 allele count, severity of Aβ neuropathology and comorbid cerebrovascular pathology may be relevant for clinicians prescribing anti-Aβ monoclonal antibodies for early AD and developing individualized safety monitoring plans.
Why it matters
This analysis of the GRADUATE I/II trials found that besides APOE ε4 allele count, severity of amyloid neuropathology and comorbid cerebrovascular pathology may be relevant for safety monitoring with anti-amyloid monoclonal antibodies in early Alzheimer's disease. It focuses on safety monitoring rather than showing a cure or prevention.
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This meta-analysis pooled 30 studies (nearly 9,800 people from 10 countries) to see how well p-tau217 measured in blood or spinal fluid detects Alzheimer's amyloid and tau pathology compared with PET scans.
Why it matters
A blood test for p-tau217 detected amyloid buildup with about 82% sensitivity and 86% specificity, similar to the more invasive spinal fluid test. This supports using blood p-tau217 as a less invasive way to identify Alzheimer's pathology, though it is a diagnostic accuracy review, not a treatment or cure.
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Of a total 912 participants, there were 499 males (54.7%) and 413 females (45.3%), and the mean (SD) age was 71.1 (8.49) years.
Why it matters
Plasma p-tau217 was most strongly associated with amyloid positivity and performed best among the biomarkers tested, with high sensitivity and specificity, and results were validated in an independent cohort. This suggests plasma p-tau217 could help select patients with Alzheimer's disease for antiamyloid immunotherapies.
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Cost-effective strategies for identifying amyloid-β (Aβ) positivity in patients with cognitive impairment are urgently needed with recent approvals of anti-Aβ immunotherapies for Alzheimer's disease (AD).
Why it matters
A two-step workflow using a plasma p-tau217-based model to stratify patients with mild cognitive impairment achieved 88.2% to 92.0% accuracy for detecting amyloid-PET status while reducing needed cerebrospinal fluid tests by 61.2% to 85.9%. This could make diagnostic testing more cost-effective, though it was evaluated in memory clinic cohorts.
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This was, at the time, the largest genetic study of Alzheimer's disease ever done, comparing DNA from over 111,000 people with the disease (or a strong family history) to nearly 680,000 people without it.
Why it matters
This was, at the time, the largest genetic study of Alzheimer's disease ever done, comparing DNA from over 111,000 people with the disease (or a strong family history) to nearly 680,000 people without it. It found 75 spots in the genome linked to Alzheimer's risk, 42 of them newly discovered, and pointed to the brain's immune cells (microglia) and amyloid/tau biology as central to disease risk, beyond the well-known APOE gene.
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Among 1431 participants, the mean (SD) age was 71.2 (8.8) years; 751 (52.5%) were male.
Why it matters
In 1,431 people from 8 cohorts in South Korea, Sweden and the US, ranging from cognitively unimpaired to Alzheimer dementia, baseline tau PET predicted change in MMSE scores over about 2 years more strongly than MRI cortical thickness or amyloid PET (R² 0.35 vs 0.24 vs 0.17 across all participants). The authors call tau PET "a promising tool for predicting cognitive change" that "may support the prognostic process" in early-stage Alzheimer's. This record does not include the results for each stage separately or for the replication cohort, and the study did not test any treatment.
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Mean age was 83.5 (SD, 8.5) years in cohort 1, 69.1 (SD, 10.3) years in cohort 2, and 35.8 (SD, 10.7) years in cohort 3; 38% were women in cohort 1, 51% in cohort 2, and 57% in cohort 3.
Why it matters
In three cohorts, plasma P-tau217 distinguished Alzheimer's disease from other neurodegenerative disorders with higher accuracy than some other blood markers. This is a diagnostic accuracy study, not a treatment or cure.
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A healthy lifestyle as a composite score is associated with a substantially lower risk of Alzheimer's dementia.
Why it matters
In these two cohorts, a higher healthy lifestyle score was linked to lower risk of Alzheimer dementia, with risk 60% lower in those with 4 to 5 healthy factors compared with 0 to 1. This is an observational association and does not prove that lifestyle changes prevent Alzheimer's disease.
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This clinical trial evaluates the efficacy and safety of a 6-week course of daily neuroAD™ therapy.
Why it matters
This randomized, sham-controlled trial tested a 6-week course of combined transcranial magnetic stimulation and cognitive training in 131 patients with Alzheimer's disease. It evaluates one treatment approach but does not establish a cure or prevention.
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77/100
An antecedent rise in Aβ was associated with subsequent changes in tau (1.07 flortaucipir standardized uptake value ratios [SUVr]/PiB-SUVr; 95% CI, 0.13-3.46; P = .02).
Why it matters
Over about 7 years in 60 older adults (median age 73) at the preclinical stage of Alzheimer's, an earlier rise in amyloid on brain scans was associated with later changes in tau, and tau changes were associated with declining thinking scores. A statistical model linked starting amyloid to cognition 7 years later through these successive changes, a pattern consistent with amyloid coming first, then tau, then decline, though it shows association, not cause. The authors say this supports repeated tau-PET to track progression and repeated amyloid-PET to spot the earliest changes; no treatment was tested.
From across this topic
10 of the 5,374 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Effect of tacrine on language, praxis, and noncognitive behavioral problems in Alzheimer disease
- Glial Cell-Mediated Neuroinflammation in Alzheimer's Disease
- Cerebrospinal fluid A beta42 is increased early in sporadic Alzheimer's disease and declines with disease progression
- Kinetic Modeling of Amyloid Binding in Humans using PET Imaging and Pittsburgh Compound-B
- MAPT STUDY: A MULTIDOMAIN APPROACH FOR PREVENTING ALZHEIMER'S DISEASE: DESIGN AND BASELINE DATA
- Alzheimer's disease: Targeting the Cholinergic System
- The role of brain MR and FDG-PET in the diagnosis of neurodegenerative disease
- Immune hyperreactivity of Aβ plaque-associated microglia in Alzheimer's disease
- Clinical diagnosis of Alzheimer's disease: Report of the NINCDS—ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease
- MRI of hippocampal volume loss in early Alzheimer's disease in relation to ApoE genotype and biomarkers