28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Genetic risk factors of AD dementia demonstrate effects related to Aβ, as well as synergistic interactions with Aβ. 2 key findings →
Design: longitudinal study Participants: 702 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Secondary analysis suggested that this effect may be driven primarily by individuals who are negative for the established AD genetic risk factor, apolipoprotein E (APOE) ɛ4. 5 key findings →
Design: case-control study Participants: 346 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the evaluated parameters, the only significant predictor of conversion to AD was non-Cp copper (hazard ratio = 1.23, 95% confidence interval = 1.03-1.47, p = 0.022); for each additional micromole per liter unit (μmol/l) of non-Cp copper, the hazard increased by ~20%. 2 key findings →
Design: meta-analysis Participants: 42 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Researchers isolated transcripts from a chromosomal region linked to an aggressive form of Alzheimer's disease and identified a novel gene transcript. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The genetic underpinnings of Alzheimer's disease (AD) remain largely elusive despite early successes in identifying three genes that cause early-onset familial AD (those that encode amyloid precursor protein (APP) and the presenilins (PSEN1 and PSEN2)), and one genetic risk factor for late-onset AD (the gene that encodes apolipoprotein E (APOE)). 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Obesity and diabetes significantly and independently increase risk for AD. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Variants in GBA, encoding the enzyme glucocerebrosidase, are associated with Lewy body diseases such as Parkinson's disease and Lewy body dementia. 5 key findings →
Design: case-control study Participants: 165 Evidence: moderate
Full summary, score breakdown and related studies → Original source
No variant passed the genome-wide significance threshold (p = 5 × 10- 8) in the case-control GWAS. 5 key findings →
Design: case-control study Participants: 285 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 463,447 TPMI participants, 4381 PD patients and 43,810 controls were analysed. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In cross-sectional analyses at baseline, there was no association between DNAm age acceleration and cognitive function scores. 5 key findings →
Design: cross-sectional Participants: 266 Evidence: moderate
Full summary, score breakdown and related studies → Original source
By wave, compared with those who remained in the LBC1921 study at Waves 1 to 5, participants who dropped out had: significantly lower older-age IQ scores at Wave 1 Wave 2 = and Wave 3 = lower scores at Waves and at Waves 1 = and 2 = By wave, compared with those who remained in the LBC1936 study at Waves 1 to participants who dropped out had: significantly lower older-age IQ scores at Wave 1 Wave 2 = and Wave 3 = lower scores at Wave 1 = Wave 2 and Wave 3 = lower at Wave 1 = Wave 2 = and Wave 3 and lower physical as at Wave 1 Wave 2 = and Wave 3 = and at Wave 1 = at each wave in the Lothian Birth Cohort 1921 are mean and standard for and for each wave sample = Wave 1 = Waves 1 and 2 = Waves 2 and 3 = Waves IQ from Moray House Test for age in at time of testing and to IQ is the was from to from the in 1 and at Wave 1. as of from the Wave 2 two participants who not Wave 1. 1 key finding →
Design: longitudinal study Participants: 87 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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. 5 key findings →
Design: cohort Participants: 9,496 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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. 3 key findings →
Design: cross-sectional Participants: 2,268 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Aβ deposition increases slowly from cognitive normality to moderate severity DAT. 5 key findings →
Participants: 206 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Longitudinal fMRI provides a reliable indicator of brain activation over time, and may prove useful in identifying functional brain changes associated with cognitive decline on the trajectory toward clinical Alzheimer disease. 3 key findings →
Design: cross-sectional Participants: 21 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Median (interquartile range) CRP levels increased with mean (SD) age (43.3 [9.6] years, 0.95 mg/L [0.40-2.35 mg/L] vs 59.1 [9.6] years, 2.04 mg/L [0.93-4.75 mg/L] vs 61.6 [9.5] years, 2.21 mg/L [1.05-5.12 mg/L]; P Conclusions and relevance In this study, peripheral chronic low-grade inflammation in participants with ApoE4 was associated with shortened latency for onset of AD. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Risk information for Alzheimer disease (AD) may be communicated through susceptibility gene disclosure, even though this is not currently in clinical use. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The ApoE ε4 allele is the most significant genetic risk factor for late-onset Alzheimer disease. 4 key findings →
Participants: 1,766 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Employing time-dependent proportional hazards modeling, the authors found no significant association between statin use and incident dementia or probable AD. 2 key findings →
Design: cohort study Participants: 312 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Overall, cumulative incidence was uniformly higher in NACC than in the population-based cohorts. 3 key findings →
Participants: 5,073 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
By conditioning on the genetic association with the cardiovascular phenotypes, we identify novel AD susceptibility loci, including 2 genome-wide significant variants conferring increased risk for AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
More research is needed to elucidate the neural mechanisms underlying these regional associations, which may involve motor and sensorimotor circuits hitherto largely neglected in the pathophysiology of AD. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic variants within the VCAN gene may play a role in the mechanisms underlying microstructural integrity of the white matter in the brain measured as FA and MD. 4 key findings →
Design: cohort study Participants: 8,448 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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). 5 key findings →
Design: cohort study Participants: 602 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 3414 included individuals, the mean (SD) age was 68.8 (6.0) years and 2116 (62%) were female. 5 key findings →
Design: cohort study Participants: 1,184 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 28,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →