Many drugs that target amyloid-β (Aβ) in Alzheimer disease (AD) have failed to demonstrate clinical efficacy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Many drugs that target amyloid-β (Aβ) in Alzheimer disease (AD) have failed to demonstrate clinical efficacy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There are few validated fluid biomarkers in frontotemporal dementia (FTD). 4 key findings →
Participants: 469 Evidence: low
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No treatment for frontotemporal dementia (FTD), the second most common type of early-onset dementia, is available, but therapeutics are being investigated to target the 2 main proteins associated with FTD pathological subtypes: TDP-43 (FTLD-TDP) and tau (FTLD-tau). 4 key findings →
Evidence: moderate
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In total, 41 participants consented (n=10, 24% participants with Alzheimer disease; n=11, 27% participants with Lewy body disease; and n=20, 49% controls). 5 key findings →
Design: longitudinal study Participants: 41 Evidence: moderate
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Evidence links air pollution to dementia, yet its role in Lewy body dementia (LBD) remains unclear. 2 key findings →
Evidence: moderate
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Light Gradient-boosting Machine (LightGBM) achieved the highest performance in identifying agitation over an 8-day period with a sensitivity of 71.32% ± 7.38 and specificity of 75.28% ± 7.38. 5 key findings →
Design: longitudinal study Participants: 63 Evidence: moderate
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We present a comprehensive global analysis of genetic variants associated with autosomal-dominant Alzheimer's disease (ADAD). 2 key findings →
Participants: 550 Evidence: low
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We recruited 210 participants; 205 (66.8% male; aged 66.4±11.1 years) had useable data. 5 key findings →
Design: longitudinal study Participants: 210 Evidence: moderate
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Collectively, plasma biomarker findings in the low p-tau217 subgroup were more robust than in the mITT population. 5 key findings →
Design: clinical trial Evidence: high
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This study estimated the utilization and lifetime costs of formal care for AD dementia using longitudinal register data. 4 key findings →
Design: cohort Participants: 20,366 Evidence: high
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Disease staging, whereby the spatial extent and load of brain pathology are used to estimate the severity of Alzheimer disease (AD), is pivotal to the gold-standard neuropathological diagnosis of AD. 5 key findings →
Evidence: low
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The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. 3 key findings →
Participants: 559 Evidence: low
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The incidence of stroke and dementia are diverging across the world, rising for those in low- and middle-income countries and falling in those in high-income countries. 3 key findings →
Evidence: low
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With the increase in large multimodal cohorts and high-throughput technologies, the potential for discovering novel biomarkers is no longer limited by data set size. 5 key findings →
Evidence: moderate
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Between May 28, 2015, and Jan 10, 2018, 502 individuals were assessed as part of Insight 46. 5 key findings →
Participants: 456 Evidence: moderate
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Two genetic variants in strong linkage disequilibrium (rs9536314 and rs9527025) in the Klotho (KL) gene, encoding a transmembrane protein, implicated in longevity and associated with brain resilience during normal aging, were recently shown to be associated with Alzheimer disease (AD) risk in cognitively normal participants who are APOE ε4 carriers. 4 key findings →
Participants: 5,541 Evidence: low
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A possible involvement of the gene IL1RAP (interleukin-1 receptor-associated protein) in the pathogenesis of Alzheimer's disease (AD) has been suggested in GWASs of cerebrospinal fluid (CSF) tau levels and longitudinal change in brain amyloid burden. 4 key findings →
Design: longitudinal study Participants: 3,446 Evidence: moderate
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Despite advances in uncovering the mechanisms that underlie neuroinflammation and neurodegenerative disease, therapies that prevent neuronal loss remain elusive. 4 key findings →
Evidence: low
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Dementia is a rapidly rising global health crisis that silently disables families and ends lives and livelihoods around the world. 4 key findings →
Evidence: low
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Among 4080 participants included in the analysis, the mean (SD) age was 66.5 (8.9) years, and 2241 (54.9%) were female. 5 key findings →
Design: cross-sectional Participants: 4,080 Evidence: low
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Baseline plasma NfL was associated with increased risk of dementia/death in the entire cohort. 4 key findings →
Design: longitudinal study Participants: 131 Evidence: moderate
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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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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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The results showed different pattern of APOE contribution in PRS risk predictions of AD/MCI and amyloid deposition. 3 key findings →
Evidence: moderate
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'Covert' cerebral small vessel disease (ccSVD) is common on neuroimaging in persons without overt neurological manifestations, and increases the risk of future stroke, cognitive impairment, dependency, and death. 3 key findings →
Evidence: high
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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 →