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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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.
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Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase.
Why it matters
In autosomal dominant Alzheimer's disease, cerebrospinal fluid and plasma neurofilament light chain trajectories were similar at presymptomatic stages and discriminated mutation carriers from non-carrier controls 10-20 years before estimated symptom onset, but after symptom onset the rate of change in cerebrospinal fluid continued to increase while the rate in plasma leveled off. Both plasma and cerebrospinal fluid changes were associated with grey-matter atrophy but not with Aβ-PET changes, supporting neurofilament light chain in both fluids as an early marker of neurodegeneration, though this concerns monitoring rather than treatment, cure, or prevention.
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Mean annual costs for individuals with clinically diagnosed AD were SEK 99,906, SEK 290,972, SEK 479,524, and SEK 795,617 in mild cognitive impairment (MCI), mild, moderate, and severe AD.
Why it matters
This registry-based cohort study found mean annual costs for individuals with clinically diagnosed Alzheimer's disease of SEK 99,906 in mild cognitive impairment, SEK 290,972 in mild, SEK 479,524 in moderate, and SEK 795,617 in severe disease. It describes costs by severity and does not test any treatment, cure, or prevention.
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63/100
It remains unclear which risk factors accelerate brain atrophy along with a progression from normal cognition to mild cognitive impairment (MCI).
Why it matters
Using long-term data from middle-aged and older adults, this cohort study examined which risk factors are linked to faster brain atrophy and progression from normal cognition to mild cognitive impairment. It identifies associations over time but does not show that changing these factors prevents progression.
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A summary measure of γ-secretase activity (γ-secretase composite [GSC]) was calculated for each variant and compared with clinical history-derived AAO using correlation analyses.
Why it matters
In people with inherited (autosomal dominant) Alzheimer's caused by PSEN1 variants, lower activity of γ-secretase, an enzyme involved in making amyloid β, was associated with earlier age at symptom onset. The authors suggest this partly explains clinical differences between people with the inherited form, support targeting γ-secretase as a treatment approach, and propose cell-based models to help predict when symptoms will start.
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We constructed models for MCI and mild dementia that predict MMSE over time.
Why it matters
This study built models using data from 961 amyloid-positive participants with mild cognitive impairment or mild dementia to predict cognitive decline over time. It is a prediction modeling study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Across the cohort of 212 individuals with SCD+ (M(Age) = 69.17 years, F 42.45%), 258 individuals with MCI (M(Age) = 72.93, F 43.80%), and 195 individuals with dementia (M(Age) = 74.07, F 48.72%), no main effect of education (ß = 0.52, 95% CI -0.30 to 1.58), but a significant education-by-group interaction on CL values, was found ( p = 0.024) using linear regression modeling.
Why it matters
Across people with subjective cognitive decline, mild cognitive impairment, and dementia, years of education showed no overall link to amyloid burden, though there was an interaction with group. The study only examines an association with amyloid and does not test any treatment, cure, or prevention.
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Differential eligibility may contribute to underrepresentation of some minoritized racial and ethnic groups in early AD trials.
Why it matters
This analysis of screening data from four trials found that Hispanic, Black, and Asian participants had higher probabilities of being ineligible for amyloid biomarker criteria than non-Hispanic White participants. This concerns fairness in who can join Alzheimer's trials, not treating, curing, or preventing the disease.
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Mild cognitive impairment (MCI) is often considered an early stage of dementia, with estimated rates of progression to dementia up to 80-90% after approximately 6 years from the initial diagnosis.
Why it matters
Working out whether mild memory problems are caused by Alzheimer's usually needs spinal-fluid tests or brain scans, which the authors note only "a limited percentage of the population" can access. This review of 29 studies found that researchers increasingly combine blood, spinal-fluid or saliva markers with brain imaging, memory tests and genetics in machine-learning models, an approach the authors say "has shown promise" but which is not yet a proven diagnostic test. They call for cheaper, long-term data from culturally diverse populations and for "white-box" (interpretable) models.
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Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes.
Why it matters
In 771 participants, higher cerebrospinal fluid PDGFRβ was related to higher age and was studied in relation to blood-brain barrier damage, neuroinflammation and Alzheimer pathologic changes. This is an observational biomarker study and does not report a treatment, cure or prevention.
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.
- 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
- Positron Emission Tomography Imaging With [18F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes
- Association of higher levels of high-density lipoprotein cholesterol in elderly individuals and lower risk of late-onset Alzheimer disease
- Predictors of Antiamyloid Medication Utilization and Adherence Among People With Alzheimer Disease and Mild Cognitive Impairment
- Soluble pool of A? amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease
- The Effect of APOE ε4 on Alzheimer's Disease Fluid Biomarkers: A Cross-Sectional Study Based on the COAST
- Small molecule therapeutics for tauopathy in Alzheimer's disease: Walking on the path of most resistance