28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Midlife NAFLD shows associations with AD and accumulating vascular pathology, revealing potential pathways linking liver function to dementia. 2 key findings →
Participants: 1,706 Evidence: low
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The reliable worsening method produced a cut point only for amyloid PET. 5 key findings →
Evidence: low
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Lecanemab significantly attenuated cognitive decline versus ADNI. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
In MCI, specific aspects of SCD severity and quality are related to CSF biomarkers indicative of AD. 3 key findings →
Design: cross-sectional Participants: 245 Evidence: low
Full summary, score breakdown and related studies → Original source
Positron emission tomography (PET) of brain amyloid b is a technology that is becoming more available, but its clinical utility in medical practice requires careful definition. 5 key findings →
Evidence: low
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Our results suggest that reactive astrogliosis, as indicated by different fluid biomarkers, influences the pathogenic cascade during the preclinical stage of AD. 2 key findings →
Evidence: low
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Regions with high-average SUVR are not necessarily those with the greatest tau pathology. 1 key finding →
Participants: 490 Evidence: low
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Similar to findings in adult mutation carriers, in the later preclinical and clinical stages of ADAD, mutation-carrying children were distinguished from control individuals by significantly higher plasma Aβ1-42 levels (mean [SD]: carriers, 18.8 [5.1] pg/mL and noncarriers, 13.1 [3.2] pg/mL; P Conclusions and relevance Children at genetic risk for ADAD have functional and structural brain changes and abnormal levels of plasma Aβ1-42. 2 key findings →
Design: cross-sectional Evidence: low
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Amyloid PET and sleep duration information was acquired on 4425 cognitively unimpaired participants (mean [SD] age, 71.3 [4.7] years; 2628 [59.4%] female; 1509 [34.1%] tested Aβ positive). 4 key findings →
Design: cross-sectional Evidence: low
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Lower PiB uptake accurately distinguishes cases with LBD from cases with AD or mixed pathology, correlating with the Thal Aβ phase. 2 key findings →
Participants: 39 Evidence: low
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Blood-based biomarkers offer a major advance in the clinical evaluation of neurodegenerative diseases. 5 key findings →
Evidence: low
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We found increased levels of YKL-40 and decreased levels of sAPPβ in both FTD and ALS groups compared to controls. 2 key findings →
Design: cross-sectional Participants: 86 Evidence: low
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Regional sex-related differences in tau PET burden may contribute to the disparities in AD prevalence between males and females. 4 key findings →
Design: cross-sectional Participants: 148 Evidence: moderate
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These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
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In addition, hippocampal sclerosis was a common neuropathological comorbidity ( n = 5) and associated with limbic-predominant TDP-43 proteinopathy ( n = 4) or FTLD-TDP ( n = 1). 1 key finding →
Design: longitudinal study Evidence: moderate
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This study suggests that information obtained from evaluating a subgroup of AD or MCI subject using second-generation TSPO tracers can be translated to the entire AD and MCI population. 5 key findings →
Design: longitudinal study Participants: 798 Evidence: moderate
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Aβ(+) patients with TES (N = 10), but not Aβ(-) TES, had significantly higher plasma P-tau levels than HC (P-tau181: p d = 1.34; P-tau217: p d = 1.59). 3 key findings →
Participants: 18 Evidence: low
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CSF p-tau181 was increased in patients with NIID without amyloid accumulation. 4 key findings →
Participants: 12 Evidence: low
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These results suggest that the presence of objective memory impairment in patients with probable CAA could serve as a marker for underlying tau pathology. 4 key findings →
Design: cross-sectional Participants: 39 Evidence: low
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Age-related frailty and disease-related frailty may represent different degrees of frailty severity on a biological level. 5 key findings →
Design: cross-sectional Participants: 1,199 Evidence: low
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Individuals with DS were more likely to have microbleeds than controls (20% vs 8.9%, p 60 years) and AD clinical stage (12.42% asymptomatic, 27.9% prodromal, 35.09% dementia) were more common in APOE ε4 carriers (26% vs 18.3% noncarriers, p = 0.008), but not associated with vascular risk factors ( p > 0.05). 4 key findings →
Design: cross-sectional Participants: 276 Evidence: low
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Participants were 60 (range 44-74) years old with 38 (30-51) years' T1D duration. 3 key findings →
Participants: 373 Evidence: moderate
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The findings do not support an effect of the exercise intervention on a single measure of neurodegeneration in AD. 2 key findings →
Participants: 136 Evidence: high
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In 7989 cognitively unimpaired participants (median [range] age, 54 [30-90] years; 4877 [61.3%] female; mean [SD] BMI, 25.9 [4.2]; mean [SD] eGFR, 80.7 [14.7] mL/min/1.73 m2), older age, lower BMI, and reduced kidney function were associated with increased NfL and GFAP concentrations; female sex was associated with increased GFAP concentrations. 5 key findings →
Design: cross-sectional Participants: 179 Evidence: low
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< 0.001). Stage-specific tau-PET region-of-interest selection reduced required sample sizes by 30%-93% for detecting hypothetical disease-modifying drug effects. 4 key findings →
Design: longitudinal study 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 →