27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline. 5 key findings →
Design: cohort Participants: 2,684 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid NFL concentration (median [interquartile range]) was higher in the AD dementia group (1479 [1134-1842] pg/mL), stable MCI group (no progression to AD during follow-up; 1182 [923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during follow-up; 1336 [1061-1693] pg/mL) compared with control participants (1047 [809-1265] pg/mL) (P Conclusions and relevance Cerebrospinal fluid NFL concentration is increased by the early clinical stage of AD and is associated with cognitive deterioration and structural brain changes over time. 2 key findings →
Design: longitudinal study Participants: 95 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neurofilament proteins have been validated as specific body fluid biomarkers of neuro-axonal injury. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Aggregated insoluble tau is one of two defining features of Alzheimer's disease. 3 key findings →
Participants: 448 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 641 participants with CSF Aβ42 data and at least two 18F-florbetapir scans, 335 (52.3%) were male. 4 key findings →
Design: cohort study Participants: 402 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma Aβ42/Aβ40 is a robust measure for detecting amyloid plaques and can be utilized to aid in the diagnosis of AD, identify those at risk for future dementia due to AD, and improve the diversity of populations enrolled in AD research and clinical trials. 3 key findings →
Participants: 465 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Both high baseline GFAP (hazard ratio 3·6, 95% CI 2·2-5·7; p 42/40 , both GFAP (2·6, 1·4-5·0; p=0·0026) and amyloid β 42/40 (2·1, 1·2-3·6; p=0·0091) were independently associated with incident dementia whereas NfL was not (1·4, 0·8-2·5; p=0·28). 2 key findings →
Design: cohort study Participants: 300 Evidence: moderate
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Our findings show that different AT(N) variants are not interchangeable, and that optimal variants differ by clinical stage. 4 key findings →
Design: longitudinal study Participants: 490 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Most neuroinflammatory CSF biomarkers were associated with WML in individuals without dementia. 5 key findings →
Design: longitudinal study Participants: 247 Evidence: moderate
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Among community-dwelling adults included in this study, higher fragmentation of the 24-hour activity rhythms was associated with greater subsequent Aβ burden, especially in APOE4 carriers. 5 key findings →
Design: cohort study Participants: 639 Evidence: moderate
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Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →
Design: cohort study Participants: 137 Evidence: moderate
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CSF A beta(1-42) was the most sensitive biomarker for AD in the autopsy cohort of CSF samples: receiver operating characteristic area under the curve of 0.913 and sensitivity for AD detection of 96.4%. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Several promising plasma biomarkers for Alzheimer's disease have been recently developed, but their neuropathological correlates have not yet been fully determined. 2 key findings →
Design: longitudinal study Participants: 105 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This large study shows the role of plasma biomarkers in differentiating patients with different dementias, and at monitoring longitudinal change. 5 key findings →
Design: longitudinal study Participants: 300 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Data from 362 study participants were analyzed (mean [SD] age, 65.6 [7.9] years), of whom 152 (42.0%) were African American, 230 (63.5%) were women, and 189 (52.2%) had MCI. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results demonstrate the feasibility and potential of immunoassay-based multiplexing to provide a comprehensive view of AD-associated proteomic changes, consistent with the recently revised biological and diagnostic framework. 5 key findings →
Design: cross-sectional Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma Aβ42/Aβ40${{\rm A}\beta }_{42}/{{\rm A}\beta }_{40}$ may begin declining decades prior to brain amyloid accumulation, whereas p-tau ratios, GFAP, and NfL increase closer in time. 1 key finding →
Design: longitudinal study Participants: 199 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 93 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study confirms the role of NFL as a biomarker in ALS. 3 key findings →
Design: longitudinal study Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The development of blood-based biomarkers of Alzheimer's disease (AD) pathology as tools for screening the general population is essential, but persists controversies. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
We believe that ours is the largest blood biomarker study of preclinical AD to date. 3 key findings →
Design: longitudinal study Participants: 28 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Astrocytes are the most abundant cell type in the human central nervous system, and they play an important role in the regulation of neuronal physiology. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma markers can track biological change over time, with plasma pTau181 and GFAP markers showing longitudinal change in individuals with preclinical AD. 3 key findings →
Design: longitudinal study Participants: 373 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The use of PRSs may be beneficial for increased precision in risk estimates among APOE4 carriers. 3 key findings →
Design: cohort study Participants: 712 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Biomarkers were measured in 431 Black and 583 White participants (mean age of 77 and 80 years and 17% and 21% of men, respectively), generating a balanced sample of 366:366. 3 key findings →
Design: cohort Participants: 1,014 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 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 →