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 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Efficacy analysis included 416 patients.
Why it matters
In 416 analyzed nursing home residents with Alzheimer's disease and psychosis, both risperidone and placebo groups improved on psychosis and global change measures with no significant difference between groups, and the trial did not confirm earlier findings. It did not show that risperidone treats psychosis of Alzheimer's disease better than placebo.
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In the largest twin study to date, we confirmed that heritability for AD is high and that the same genetic factors are influential for both men and women.
Why it matters
In all twins aged 65 and over in the Swedish Twin Registry (11,884 pairs, 392 with Alzheimer's in one or both twins), genetic differences accounted for an estimated 58% to 79% of the variation in who developed Alzheimer's, depending on the model. The rest was attributed to environmental factors not shared by twins. Heritability did not differ significantly between men and women, and the timing of onset also appeared to be partly genetic. These are population-level estimates from one country, not a measure of any individual's risk, and the study does not identify genes or test any treatment.
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Vascular and inflammatory factors may play an important role in the pathogenesis of dementia.
Why it matters
This study investigated whether the inflammatory and clotting marker fibrinogen, and C-reactive protein, are associated with dementia. It is about a possible risk marker, not about treating, curing or preventing Alzheimer's disease.
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This multicenter trial showed no benefit of divalproex sodium for treatment for agitation in dementia at a mean dose of 800 mg/day over 6 weeks.
Why it matters
In this 6-week randomized, double-blind, placebo-controlled trial of 153 nursing home residents with Alzheimer disease and agitation, divalproex sodium did not differ from placebo on the primary agitation measure or on secondary behavioral measures. The results do not support findings from previous trials indicating possible benefit.
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A four month, parallel group, placebo controlled trial undertaken in three centres in Tehran, Iran.
Why it matters
In this four-month placebo-controlled trial of 42 people with mild to moderate Alzheimer's disease, Melissa officinalis extract produced significantly better cognitive function than placebo and had a positive effect on agitation. This suggests a possible benefit for managing symptoms, but it does not show that the extract cures or prevents Alzheimer's disease.
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Type 2 diabetes may be a risk factor for dementia, but the associated pathological mechanisms remains unclear.
Why it matters
In this cohort, type 2 diabetes was associated with higher risk of total dementia, Alzheimer's disease, and vascular dementia, and men with both diabetes and the APOE epsilon4 allele had a much higher risk of Alzheimer's disease. It identifies diabetes and the APOE epsilon4 allele as risk factors but does not show that treating diabetes prevents or cures Alzheimer's disease.
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As galantamine slowed the decline of functional ability as well as cognition, its effects are likely to be clinically relevant.
Why it matters
In this six-month randomized trial of 653 patients, galantamine produced significantly better cognitive outcomes than placebo in mild to moderate Alzheimer's disease and also slowed decline in functional ability. This is a symptomatic treatment effect, not a cure or prevention.
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Researchers isolated transcripts from a chromosomal region linked to an aggressive form of Alzheimer's disease and identified a novel gene transcript.
Why it matters
Reports the cloning of a gene carrying missense mutations in early-onset familial Alzheimer's disease. Identifying such a gene gives researchers something concrete to study, but is not a treatment or a way to prevent the disease.
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Donanemab, a monoclonal antibody targeting the insoluble form of β-amyloid found in plaques, significantly slows cognitive and functional decline of AD in participants with mild cognitive impairment (MCI) or mild AD-related dementia.
Why it matters
In this Phase 3 trial, donanemab reduced the risk of progression from mild cognitive impairment to mild Alzheimer's disease by 33% and from mild to moderate Alzheimer's disease by 50%. These results support clinically meaningful effects on cognition and function for patients with early symptomatic Alzheimer's disease.
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Of 2,323 MEMENTO participants, 2,136 (92%) were included in this study.
Why it matters
In outpatients with mild cognitive symptoms, probable CAA by Boston criteria V1.5 but not V2.0 was associated with increased risk of dementia, and this association was not significant when further adjusting for APOE ε4. The authors call for external validation, and no treatment, cure or prevention is reported.
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Female individuals had higher plaque burden than male individuals (unadjusted odds ratio [OR], 1.97; 95% CI, 1.67-2.29; P Conclusions and relevance The findings indicate that female sex, APOEε4, and both race and African ancestry were jointly associated with amyloid in this study population.
Why it matters
In this autopsy study from Brazil, women had higher neuritic plaque burden than men, and the findings indicate that female sex, APOE ε4, and other factors interact in Alzheimer disease pathology. Because it examines brain tissue after death, it helps explain differences in disease biology but does not test any treatment or prevention.
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Among 3414 included individuals, the mean (SD) age was 68.8 (6.0) years and 2116 (62%) were female.
Why it matters
Learning an elevated amyloid result or APOE ε4 homozygosity was linked to higher short-term intrusive thoughts, though group average distress scores stayed below clinically significant thresholds. The findings concern the psychological impact of disclosure and do not address treating, curing, or preventing Alzheimer disease.
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This study highlights challenges for the reproducibility of α-syn SAA results across different protocols applied by different laboratories.
Why it matters
This study tested the α-synuclein seed amplification assay for diagnosing dementia with Lewy bodies across four laboratories using CSF samples from 20 patients and 10 controls. Diagnostic performance varied widely across laboratories, with sensitivity ranging from 55% to 100% and specificity from 60% to 100%, highlighting challenges for reproducibility.
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Benefit continued to accrue with ongoing lecanemab treatment through 36 months.
Why it matters
In this open-label extension, participants continued to benefit from lecanemab through 36 months, and ARIA rates were low after 6 months. Results in the low pathology subgroup support early initiation of lecanemab treatment.
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The apolipoprotein E (APOE) gene is the best established genetic risk factor for Alzheimer's disease in later life, with the ε4 allele conferring higher risk.
Why it matters
This study found that disclosing APOE genotype to cognitively unimpaired, psychologically pre-screened adults by a trained health-care provider was generally safe and well tolerated. Disease-specific distress 2-7 days after disclosure increased more in homozygotes than in heterozygotes, and the authors say the results may be useful for clinical disclosure programmes.
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Studies evaluating the diagnostic test accuracy of plasma phosphorylated tau (p-tau) and amyloid beta (Aβ) tests (p-tau217, %p-tau217, p-tau181, p-tau231, and Aβ42/Aβ40) compared to reference standard tests (cerebrospinal fluid [CSF] AD biomarkers, amyloid positron emission tomography [PET], or neuropathology) in individuals with cognitive impairment (mild cognitive impairment or dementia) in specialized care settings were included.
Why it matters
This review of 49 studies examined how well plasma p-tau and amyloid beta tests detect Alzheimer's disease pathology in people with cognitive impairment in specialized care settings. It found that test performance is specific to the assay and platform used, and advises clinicians to interpret results in the context of the specific test and integrate them with a comprehensive clinical assessment.
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63/100
Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models.
Why it matters
Dividing certain Alzheimer's fluid biomarkers by reference proteins such as Aβ40 or np-tau strengthened their link to amyloid and tau PET scans in a large cohort. This is a measurement improvement that could make blood and spinal fluid tests more accurate, not a treatment or cure.
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Alzheimer's disease is a progressive neurodegenerative disorder with no cure, making preventive strategies crucial.
Why it matters
In this five-year study of 1500 people, higher adherence to the Mediterranean or MIND diet was associated with better cognitive scores and lower amyloid-beta, tau, and inflammatory markers, with the MIND diet showing a slightly stronger link. It is an observational cohort study, so it cannot prove that diet prevents or treats Alzheimer's, and APOE-ε4 carriers may respond differently.
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In a total of 602 autopsy cases (median [IQR] age at death, 78 [71-85] years; 328 male [54.5%] and 274 female [45.5%]), higher PM2.5 exposure prior to death was associated with increased odds of more severe Alzheimer disease neuropathologic change (ADNC) (odds ratio, 1.19; 95% CI, 1.11-1.28).
Why it matters
In autopsy cases, higher PM2.5 exposure before death was associated with more severe Alzheimer's disease neuropathologic change and greater cognitive and functional impairment, with much of that association mediated by ADNC. This links air pollution to dementia severity but does not test any treatment, cure, or prevention.
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Of 18 293 participants included in the parent study, scan images were available for 10 774 (59%), of which Centiloids were successfully calculated for 10 361 (96%).
Why it matters
This study reports how often amyloid PET scans could be quantified using Centiloids, with 10,361 of 10,774 available scans successfully calculated. It is a technical report about scan measurement and does not address treating, curing, or preventing Alzheimer's disease.
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A total of 807 K-ROAD participants (median age 72.0 years, 58.7% female) and 230 ADNI participants (median age 70.9 years, 49.1% female) were analyzed.
Why it matters
A two-stage workflow using MRI-based risk grouping plus plasma p-tau217 testing accurately identified amyloid PET positivity in early-stage Alzheimer's disease while reducing the need for extra biomarker tests. The authors note the improvement over baseline models was modest and the sample had limited racial and ethnic diversity.
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Obesity and Area Deprivation Index, a measure of socioeconomic status, were significantly associated with elevated AD risk within the hypertensive cohort.
Why it matters
Among people with high blood pressure, obesity and neighborhood disadvantage were linked to higher Alzheimer's risk, and six genetic variants were also associated with the disease. The authors say these findings point to obesity prevention and management as part of efforts to reduce Alzheimer's risk in this group.
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Plasma p-tau217 levels showed a significant increase across advancing AD stages, with all between-group comparisons remaining significant after false discovery rate adjustment ( p p = 0.002) and CSF p-tau181 (β = 3.2, 95% CI 1.4-5.0, p = 0.001).
Why it matters
In 731 participants followed for up to 10 years, higher plasma p-tau217 levels were associated with faster cognitive decline and progression to dementia across Alzheimer's stages. This is a prognostic biomarker study and does not test any treatment, cure, or prevention for the disease.
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Comorbid cardiovascular and metabolic risk factors (CVM) differentially impact brain structure and increase dementia risk, but their specific magnetic resonance imaging signatures (MRI) remain poorly characterized.
Why it matters
Machine learning models using MRI data from 37,096 participants identified distinct neuroanatomical signatures of cardiovascular and metabolic diseases in cognitively unimpaired individuals, with markers most sensitive in mid-life. Integrating these personalized brain signatures could guide early risk detection and stratification, but this does not treat, cure, or prevent Alzheimer's disease.
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These findings suggest that PA may help delay cognitive decline by modulating neurodegeneration and AD-specific tau pathologies.
Why it matters
In this cross-sectional study, people reporting the most physical activity had lower ptau217 and NfL levels and better cognitive scores than those reporting the least. Because it looked at one point in time, it cannot show that physical activity causes these differences or prevents Alzheimer's disease.
From across this topic
10 of the 5,172 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.
- Both common variations and rare non-synonymous substitutions and small insertion/deletions in CLU are associated with increased Alzheimer risk
- Biomarker-Based Diagnosis and Care Pathways for Alzheimer's Disease in the Era of Disease-Modifying Treatments: A Consensus Statement by Belgian Experts
- A cross-sectional study of neuropsychiatric symptoms in 435 patients with Alzheimer's disease
- Chemokines/chemokine receptors in the central nervous system and Alzheimer's disease
- A European multicentre PET study of fibrillar amyloid in Alzheimer's disease
- Alzheimer's Disease and Diabetes: Insulin Signaling as the Bridge Linking Two Pathologies
- B31-13 Circadian Rest-Activity Rhythm and Alzheimer’s Disease Biomarkers in Adults With Down Syndrome
- Microglia‐specific Alzheimer's disease polygenic risk score predicts longitudinal increase in plasma tau and faster cognitive decline in cognitively unimpaired older adults
- Correlation and Interchangeability of Amyloid, Tau, and Glucose Metabolism PET in Mild Cognitive Impairment and Alzheimer: A Review
- Deficient brain insulin signalling pathway in Alzheimer's disease and diabetes