31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
CSF SDC4 levels were elevated in AD, including the earliest preclinical stages, compared to controls and were closely associated with CSF and imaging biomarkers of amyloid and tau, and CSF biomarkers of neuronal and synaptic injury, astrocytic reactivity and microglial dysregulation. 1 key finding →
Design: cross-sectional Participants: 1,041 Evidence: moderate
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The study included 560 amyloid-positive participants (BioFINDER: n = 431; mean [SD] age, 73.6 [7.0] years; 212 female [49.2%] and 219 male [51.8%]; TRIAD: n = 129; mean [SD] age, 70.4 [8.3] years; 76 female [58.9%] and 53 male [41.1%]). 5 key findings →
Design: cohort study Participants: 431 Evidence: moderate
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Despite reductions in plasma p-tau217 with donanemab treatment, this biomarker cannot currently be used to accurately detect TRAC by PET (< 24.1 CL) in individuals with early symptomatic AD. 1 key finding →
Design: phase-3-trial Participants: 830 Evidence: null result
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Inflammation in Alzheimer's disease (AD) patients is characterized by increased cytokines and activated microglia. 2 key findings →
Evidence: low
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In all 6 patients (3 women and 3 men; mean age 61.8 years), the underlying clinical phenotype was associated with the regional distribution of the [18F]AV-1451 signal. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma biomarker results confirm cerebrospinal fluid studies reporting increased levels of pancreatic polypeptide and N-terminal protein B-type brain natriuretic peptide in patients with AD and mild cognitive impairment. 3 key findings →
Design: cohort study Evidence: moderate
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As serum NfL correlates with functional impairment and brain atrophy in bvFTD at different disease stages, we propose it as marker of disease severity, paving the way for its future use as outcome measure for clinical trials. 1 key finding →
Participants: 74 Evidence: low
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Overall visual ratings showed complete concordance between radiotracers for both the medial temporal lobe and the neocortex. 5 key findings →
Design: longitudinal study Evidence: moderate
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In this study, serum DHA levels were associated with pathogenesis of cerebral amyloidosis and with preservation of entorhinal and hippocampal volumes. 5 key findings →
Design: cross-sectional Participants: 61 Evidence: low
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In cohort 1, PVEC increased the effect on AD-versus-HC discrimination from a Cohen d value of 1.68 to 2.0 for composite SUVRs and from 0.04 to 1.04 for mesial temporal cortex SUVRs. 2 key findings →
Evidence: moderate
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LBD/A+T+ and AD cases showed significantly increased CSF levels of synaptic and neuroaxonal biomarkers compared with LBD/A-T- and control subjects. 3 key findings →
Participants: 101 Evidence: low
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Neurofilament light chain (NfL) is a promising biomarker for risk stratification and disease monitoring of dementia, but its utility in the preclinical disease stage remains uncertain. 4 key findings →
Participants: 975 Evidence: low
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Longitudinal patterns of clinical decline differ between LPA and PCA but are heterogeneous and related to different patterns of topographic spread. 5 key findings →
Design: case-control study Participants: 27 Evidence: moderate
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Novel plasma assays enabled accurate blood-based biomarkers for neurodegenerative diseases with minimally invasive options for clinical use. 5 key findings →
Participants: 3,232 Evidence: low
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Our study provides evidence that plasma p-tau217 has strong discriminative accuracy for AD among patients with early-onset and/or atypical dementia assessed in specialized settings. 4 key findings →
Participants: 81 Evidence: low
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Selected CSF biomarkers at presentation were associated with etiologic diagnoses and treatment responsiveness in patients with heterogeneous causes of RPD. 3 key findings →
Design: cross-sectional Participants: 44 Evidence: low
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Ten papers were identified from 7 studies. 5 key findings →
Design: systematic review Evidence: high
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The findings suggest that permeability of the blood-brain barrier is linked to AD pathophysiology, contributes to cerebrovascular lesions observed on MRI, and is associated with neuroinflammation in middle age. 5 key findings →
Participants: 488 Evidence: low
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In the whole cohort, p ‐tau217, NfL, GFAP and p ‐tau181 were significantly increased over time showing more accelerated increase in Aβ+ than Aβ‐ participants. 4 key findings →
Design: longitudinal study Participants: 718 Evidence: moderate
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This cross-sectional study evaluates the performance of the US Food and Drug Administration–cleared phosphorylated tau 217 (p-tau217) to β-amyloid 42 ratio cut points used to detect amyloid pathology associated with Alzheimer disease. 1 key finding →
Design: cross-sectional Evidence: low
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Plasma p‐tau 217 offers a cost‐effective AD‐specific alternative to tau‐PET and could potentially be implemented for monitoring cognitive changes in AD trials, while amyloid‐PET lacks utility. 1 key finding →
Design: longitudinal study Participants: 141 Evidence: moderate
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A total of 322 participants with p-tau217, GFAP, and NfL analyses were stratified into the EOAD or FTD group based on their diagnosis. 5 key findings →
Design: cohort study Participants: 245 Evidence: moderate
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With the increasing life expectancy in developed countries, the incidence of Alzheimer's disease (AD) and thus its socioeconomic impact are growing.
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In this real-world dataset, we identified effects of multimorbidities on plasma biomarkers, especially kidney function. 2 key findings →
Design: cross-sectional Participants: 617 Evidence: moderate
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Glial fibrillary acidic protein (GFAP) is the main astrocytic intermediate filament (IF). 1 key finding →
Evidence: low
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.
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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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 →
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