27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The analyses of the community‐based U.S. POINTER indicate that AA/B individuals present differences in AD and related dementia biomarker values. nHW had higher fully adjusted cognitive scores. 5 key findings →
Participants: 644 Evidence: low
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We found ADI*pTau217 interactions on immediate and delayed word recall. 5 key findings →
Participants: 136 Evidence: moderate
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P‐tau217/Aβ42 had the highest performance to discriminate Aβ+ from Aβ‐ (Table 1A,1B; all AUC≥0.90), and p‐tau217 showed excellent accuracy in ADNI sample (0.96; Table 1B). 2 key findings →
Participants: 213 Evidence: low
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Biomarkers serve as a quantitative measure of brain injury and may predict cognitive outcome after cardiac arrest. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PRS correlated positively with log-NFL (r = 0.31, p = 0.004) and inversely with N3 duration (r = −0.26, p = 0.017). 5 key findings →
Design: cross-sectional Participants: 84 Evidence: low
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Compared to CN, we identified 32 differential metabolites in AD and 49 in MCI serum. 5 key findings →
Participants: 22 Evidence: moderate
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For 43 assays, more than 80% of samples provided concentrations within the dynamic range of the assay. 5 key findings →
Participants: 100 Evidence: low
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We found significant main effects between GFAP groups and age, diagnosis of AD, diagnosis of VaD, MoCA, sex, CRP and BMI. 5 key findings →
Participants: 60 Evidence: low
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Alzheimer's disease is the most common form of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia worldwide. β-amyloid peptide (Aβ) is currently assumed to be the main cause of synaptic dysfunction and cognitive impairments in AD, but the molecular signaling pathways underlying its neurotoxic consequences have not yet been completely explored. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a multifactorial age-related brain disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Psychosocial stress and physical, cognitive, and social activity predict the risk of cognitive decline and dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The present study aimed to acquire more information on aging-related alterations, using proteomic and genomic analyses of hippocampus from young (8 months) and old (27 months) rats. 3 key findings →
Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia. 4 key findings →
Participants: 53 Evidence: low
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Synaptic loss is the best surrogate for cognitive decline in Alzheimer disease (AD) and is more closely associated with cognitive function than amyloid or tau pathologies. 4 key findings →
Design: cross-sectional Participants: 20 Evidence: low
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After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β = -0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1). 5 key findings →
Evidence: moderate
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Both taus are very significantly correlated ( p 0,697 in all groups), and with YKL‐40 (r>0.430). 5 key findings →
Participants: 89 Evidence: low
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Cognitive impairment associated with Aβ positivity and low tau (A+T‐) is linked to mixed AD. 3 key findings →
Participants: 77 Evidence: low
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After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β =-0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
BackgroundRecently published clinical studies suggest that blood-based biomarker tests (BBMTs) for Alzheimer's disease (AD) provide value, but in the U.S., neither public nor private payers currently cover these tests. 1 key finding →
Participants: 12 Evidence: low
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Hemostatic biomarkers were higher in Vascular group compared to Alzheimer group whereas there was no difference in inflammatory biomarkers. 5 key findings →
Participants: 68 Evidence: low
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Thirty-four years ago, amyloid-β 1-42 peptide was identified in amyloid plaques from brain tissue obtained from patients with Alzheimer disease (AD) and Down syndrome. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder with characteristic neuropathological changes of the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The presence of concomitant Alzheimer pathology has been linked to earlier death in cases with dementia with Lewy bodies (DLB). 4 key findings →
Evidence: low
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CSF biomarker studies were performed in 6 patients each with tremor-dominant (TD) and non-tremor-dominant (NT) Parkinson disease (PD) patients, 27 Alzheimer disease (AD) and 17 age-matched controls. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 829 studies in this tag, 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.
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →