We developed and validated a novel Simoa immunoassay to detect p-tau T217 in CSF. 4 key findings →
Participants: 77 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
We developed and validated a novel Simoa immunoassay to detect p-tau T217 in CSF. 4 key findings →
Participants: 77 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It is unknown whether multidomain interventions, which might preserve late-life cognition, affect Alzheimer's disease pathology. 4 key findings →
Participants: 527 Evidence: high
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It is largely unknown how alcohol use affects the risk of Alzheimer`s disease (AD). 4 key findings →
Design: cohort study Participants: 301 Evidence: moderate
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The association of testosterone concentrations with dementia risk remains uncertain. 4 key findings →
Evidence: low
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High correlations between plasma and serum were observed for most assays (ρ > 0.8), though plasma often yielded higher concentrations. 5 key findings →
Participants: 100 Evidence: low
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The final study sample comprised 8,797 participants (53.5% women, mean age at HUNT4 77.8 [SD 6.2]). 5 key findings →
Participants: 8,797 Evidence: low
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Among 203 enrolled patients, 186 (mean [SD] age, 68.7 [5.2] years; 119 males [64.0%]) were randomized (137 to the CN-105 group, 49 to the placebo group) and underwent surgery. 5 key findings →
Design: clinical trial Evidence: high
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Plasma p-tau217 showed strong diagnostic performance for distinguishing AD from bvFTD (96% accuracy) and PPD (93% accuracy). 5 key findings →
Participants: 40 Evidence: low
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Of the 250 participants, 121 (48.4%) were female and the mean age at follow-up was 76.06 (SD 0.48). 5 key findings →
Design: cohort study Participants: 250 Evidence: moderate
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We investigated whether β-amyloid, cortical thickness in medial temporal lobe structures, neuroinflammation, and sociodemographic factors were associated with greater anxious-depressive symptoms during the COVID-19 confinement. 5 key findings →
Participants: 921 Evidence: moderate
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Molecular subtypes of sporadic CJD show different levels of plasma tau. 2 key findings →
Participants: 132 Evidence: low
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Alzheimer's disease (AD), the most common form of dementia, remains challenging to understand and treat despite decades of research and clinical investigation. 3 key findings →
Evidence: low
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Although plasma pTau181, pTau217, pTau231, and GFAP were significantly associated with both Aβ-PET and CSF pTau181, Aβ-PET explained more variance in the levels of these biomarkers. 4 key findings →
Evidence: moderate
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Amyloid pathology is associated with changes in structural MRI measures in CN and MCI. 3 key findings →
Participants: 337 Evidence: low
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Gait is emerging as a potential diagnostic tool for cognitive decline. 2 key findings →
Participants: 20 Evidence: low
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Baseline tau-PET and a composite baseline cognitive score were the strongest independent predictors of cognitive decline. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. 2 key findings →
Participants: 20 Evidence: low
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The empirical language composite showed superior and consistent sensitivity (faster decline rate) with all three biomarkers. 5 key findings →
Design: longitudinal study Evidence: moderate
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One hundred forty-six participants were examined (age 72 ± 6 years). 3 key findings →
Evidence: low
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Several recent research studies show high performance of blood biomarkers to identify Alzheimer's disease also in the pre-dementia mild cognitive impairment (MCI) stage, but data from the routine clinical care memory clinic setting are needed. 1 key finding →
Participants: 54 Evidence: low
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Treatment-resistant schizophrenia does not appear to be associated with neuronal, particularly axonal degeneration. 4 key findings →
Participants: 82 Evidence: moderate
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The defining pathological features of Alzheimer disease (AD) may also be contributing factors in other dementias. 4 key findings →
Design: cross-sectional Evidence: low
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Intrinsic capacity (IC) is a recent key concept proposed by the World Health Organization (WHO) based on aspects of functional ability (both physical and mental) rather than the presence or absence of diseases, with a potential to predict several health outcomes. 4 key findings →
Design: cross-sectional Participants: 491 Evidence: low
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= 0.64). In AD-relevant regions, increased free water correlates with tau load independently of macrostructural metrics or amyloid load. 2 key findings →
Evidence: moderate
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Synaptic degeneration has been linked to cognitive decline. 5 key findings →
Participants: 187 Evidence: moderate
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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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →