27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Lower baseline amyloid beta (Aβ)42/40 ratio and higher phosphorylated tau 181 (p-tau181), glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) were associated with an increased risk of MCI and dementia; GFAP was most strongly associated. 5 key findings →
Participants: 2,467 Evidence: high
Full summary, score breakdown and related studies → Original source
A total of 18 high-quality studies comprising 24 independent datasets and 4,736 participants were included. 5 key findings →
Design: systematic review Participants: 4,736 Evidence: high
Full summary, score breakdown and related studies → Original source
A total of 24 published articles that included 2397 AD and 3242 MCI patients were analysed. 5 key findings →
Design: meta-analysis Participants: 2,397 Evidence: high
Full summary, score breakdown and related studies → Original source
A total of 917 participants had a mean baseline age of 67.4 years (SD 12.1), 49.4% were female, and 48.6% self-identified as Black. 5 key findings →
Design: cohort study Participants: 30,239 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Participants with Elevated/High %p-tau217 exhibited accelerated cognitive decline, hippocampal atrophy, and significantly higher risks of progression to MCI (hazard ratio [HR] > 6.0) and dementia (HR > 9.9). 4 key findings →
Design: longitudinal study Participants: 1,204 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma amyloid-β(Aβ)42/40 ratio, glial fibrillary acidic protein (GFAP), neurofilament light (NfL), and phosphorylated tau181(p-tau181) are promising biomarkers for Alzheimer's disease (AD)-related pathology. 3 key findings →
Design: cohort study Participants: 1,270 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The cohorts had low pre-test probability (%Aβ positivity = 14.9-24.7) and were predominantly cognitively normal (> 73%). 5 key findings →
Design: cohort study Participants: 441 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Multivariable models (p-tau+GFAP+NfL) had the best performance to detect Aβ+ in NormCog (ROCAUC = 0.87) and ImpCog (ROCAUC = 0.87). 5 key findings →
Design: longitudinal study Participants: 132 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma NfL and GFAP were associated with vascular brain damage and differed across states (VCI > vascular CU > non-vascular CI > non-vascular CU). 5 key findings →
Design: longitudinal study Participants: 1,810 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 17 articles were identified. Plasma Aβ42/40 ratio was inversely correlated with aPET positivity r = -0.48 (95% confidence interval (CI): -0.65--0.31). 5 key findings →
Design: systematic review Participants: 17 Evidence: high
Full summary, score breakdown and related studies → Original source
We identified that combining plasma p-tau217 and a brief cognitive composite score was strongly related to greater risk of progression to AD dementia in MCI patients, suggesting that these measures could be key components of future prognostic algorithms for early AD. 2 key findings →
Participants: 110 Evidence: low
Full summary, score breakdown and related studies → Original source
Phosphorylated-tau (p-tau217) is a promising blood-based biomarker for Alzheimer's dementia (AD) in clinical settings. 3 key findings →
Design: cohort study Participants: 779 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recently approved anti-amyloid immunotherapies for Alzheimer's disease (AD) require evidence of amyloid-β pathology from positron emission tomography (PET) or cerebrospinal fluid (CSF) before initiating treatment. 4 key findings →
Design: cohort study Participants: 6,896 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Alzheimer's Disease Neuroimaging Initiative (ADNI) aims to validate biomarkers for Alzheimer's disease (AD) clinical trials. 1 key finding →
Design: longitudinal study Participants: 20,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 levels decreased significantly from 3 months, with the greatest decline between 3 and 6 months, followed by a plateau. 5 key findings →
Design: longitudinal study Participants: 153 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Of 504 enrolled patients, 491 completed POD assessment (mean [SD] age, 68.4 [8.3] years; 385 [78.4%] male), of whom 106 (21.6%) developed POD. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
For Aβ42/Aβ40, cutoffs across cohorts were <0.059 (BioFINDER), <0.057 (ADNI), and <0.058 (UCSF). 5 key findings →
Design: longitudinal study Participants: 750 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This fully-automated and available blood-based biomarker assay therefore may be useful for early detection, diagnosis, prognosis, and treatment monitoring of AD. 5 key findings →
Design: longitudinal study Participants: 463 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood biomarkers have great potential to advance clinical care and accelerate trials in Alzheimer's disease (AD). 1 key finding →
Design: longitudinal study Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood biomarkers have been considered tools for the diagnosis, prognosis, and monitoring of Alzheimer's disease (AD). 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
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
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
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
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
8 of the 698 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 8. The same 8 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 27,380 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 →