27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. 4 key findings →
Design: longitudinal study Participants: 123 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood exosomes, which are extracellular vesicles secreted by living cells into the circulating blood, are regarded as a relatively noninvasive novel tool for monitoring brain physiology and disease states. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Our systematic review shows evidence for disruptions in (night-time) melatonin levels in AD as compared to age-matched controls. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Emerging plasma biomarkers of Alzheimer's disease might be non-invasive tools to trace early Alzheimer's disease-related abnormalities such as the accumulation of amyloid-beta peptides, neurofibrillary tau tangles, glial activation and neurodegeneration. 4 key findings →
Design: longitudinal study Participants: 164 Evidence: moderate
Full summary, score breakdown and related studies → Original source
More than 20 genetic loci have been associated with risk for Alzheimer's disease (AD), but reported genome-wide significant loci do not account for all the estimated heritability and provide little information about underlying biological mechanisms. 5 key findings →
Design: case-control study Participants: 3,146 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results revealed machine learning with novel biomarkers and multiple variables may increase the sensitivity and specificity in diagnosis of AD. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 showed the strongest individual association with Aβ PET status (area under the curve [AUC], 0.85). 5 key findings →
Design: cohort study Participants: 1,407 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Combining plasma p-tau with Aβ42 or the Aβ42/40 ratio reduced the intermediate zone. 5 key findings →
Design: cross-sectional Participants: 326 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuropathology cases included 46 Parkinson's disease and 10 dementia with Lewy bodies, and clinical cases included 173 Parkinson's disease, and 64 controls. 5 key findings →
Design: cohort study Participants: 46 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hallucinations, delusions, and depression were more common in DLB than in AD and, in a subgroup with longitudinal follow-up, persistent hallucinations and NPSs were associated with lower p-tau181 and p-tau231 in DLB. 5 key findings →
Design: longitudinal study Participants: 222 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Core 1 biomarker PGSs predicted AD pathology and associated cognitive performance better than the AD PGSs in both populations. 5 key findings →
Design: longitudinal study Participants: 515 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher concentrations of plasma p-tau217, p-tau181, and NfL were correlated to higher decline speed of Mini-Mental State Examination score, and higher risk of incident dementia and AD. 3 key findings →
Design: longitudinal study Participants: 1,857 Evidence: moderate
Full summary, score breakdown and related studies → Original source
None of the three plasma biomarker was associated with NPS at baseline. 5 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In general linear models lower plasma Aβ42/40 was related to lower visuospatial ability, higher total tau was related to lower episodic memory, and higher NfL was related to lower visuospatial ability and lower episodic memory. 3 key findings →
Design: cohort study Participants: 260 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A blood biomarker-based staging system for Alzheimer's disease (AD) could improve the diagnosis, prognosis and identification of individuals most likely to benefit from specific therapies. 3 key findings →
Design: longitudinal study Participants: 689 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mixed-effect models assessed rates of memory decline in relation to baseline plasma p-tau181, and whether plasma p-tau181 significantly predicted memory decline beyond widely available clinical and genetic data (age, sex, years of education, cardiovascular and metabolic conditions, and APOEε4 status). 5 key findings →
Design: longitudinal study Participants: 604 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A lack of convenient and reliable biomarkers for diagnosis and prognosis is a common challenge for neurodegenerative diseases such as Alzheimer's disease (AD). 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
This paper highlights the growing evidence that blood-based tau biomarkers have early diagnostic utility for Alzheimer's disease. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Our findings demonstrate that spindle and SO activity during sleep constitute predictive and non-invasive biomarkers of neurodegeneration and cognition in AD patients. 2 key findings →
Design: prospective cohort Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
MMP-9 may have more detrimental effects on AD-related pathological and cognitive changes in women. 4 key findings →
Design: longitudinal study Participants: 238 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Despite assumptions that cognitive changes invariably follow biomarker changes, early neuropsychological difficulties may emerge before/concurrently with plasma p-tau181 changes. 2 key findings →
Design: longitudinal study Participants: 402 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings suggest that plasma, CSF, and neuroimaging biomarkers differ considerably within the ATN framework; the most accurate target biomarkers for diagnosing AD were the CSF-A, neuroimaging-T, and neuroimaging-N within each ATN modality. 4 key findings →
Design: longitudinal study Participants: 2,340 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Physical activity is a promising preventative strategy for Alzheimer's disease: it is associated with lower dementia risk, better cognition, greater brain volume and lower brain beta-amyloid. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that plasma pTau181, plasma pTau217 and amyloid-β PET convey overlapping information and therefore predict the dynamic phase of asymptomatic amyloid-β accumulation with comparable performances. 1 key finding →
Design: cohort study Participants: 75 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In adjusted models, higher concentrations of p-tau181 (β per year 0·93 [95% CI 0·71 to 1·16]; p<0·0001), p-tau217 (β per year 1·31 [1·03 to 1·58]; p<0·0001), neurofilament light chain (β per year 0·76 [0·56 to 0·96]; p<0·0001), and GFAP (β per year 0·37 [0·21 to 0·53]; p<0·0001) were associated with an accelerated decline of chair-stand performance over time. 3 key findings →
Design: cohort study Participants: 3,363 Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 3,069 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →