28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Unlike pNfL, which was increased similarly in both clinical groups, pGFAP was increased in FTD but lower than in AD (all P < 0.01). 4 key findings →
Design: cross-sectional Participants: 211 Evidence: low
Full summary, score breakdown and related studies → Original source
Unlike familial Alzheimer's disease, we have been unable to accurately predict symptom onset in presymptomatic familial frontotemporal dementia (f-FTD) mutation carriers, which is a major hurdle to designing disease prevention trials. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma levels of glial fibrillary acidic protein (GFAP) and neurofilament light (NEFL) are key dementia biomarkers. 3 key findings →
Participants: 50,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
GFAP was lower in NB compared to prodromal AD (p = 0.003, d = 1.463) and AD-D (p = 0.002, d = 1.695). 5 key findings →
Design: cross-sectional Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
136 adults with T1D (n=90, age 52 years, 58% female, average HbA1c 7.7%) and without T1D (n=46, age 53 years, 57% female, average HbA1c 5.4%) were included. 5 key findings →
Design: cross-sectional Participants: 90 Evidence: low
Full summary, score breakdown and related studies → Original source
NfL demonstrated fair to excellent accuracy in differentiating non-ACS from CU groups (area under the curve [AUC], 0.79 to 0.94). p-tau217 had the highest accuracy for identifying Aβ (AUC 0.94) and tau positron emission tomography status (AUC 0.91). 5 key findings →
Participants: 2,984 Evidence: low
Full summary, score breakdown and related studies → Original source
In 320 patients, baseline plasma NfL levels were negatively associated with global cognition (β=-1.28 (-1.81 ; -0.75) P < 0.001), memory (β=-1.48 (-2.38 ; -0.59), P = 0.001), language (β=-1.72(-2.49 ; -0.95) P < 0.001), praxis (β=-2.02 (-2.91 ; -1.13) P < 0.001) and executive functions (β=-0.81, P < 0.001). 5 key findings →
Design: cross-sectional Participants: 158 Evidence: moderate
Full summary, score breakdown and related studies → Original source
After adjusting for age, health status, and young adult general cognitive ability, plasma NfL level was only significantly associated with processing speed and white matter hyperintensity (WMH) volume, but not with other cognitive or neuroimaging measures. 5 key findings →
Design: cross-sectional Participants: 969 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Compared to non-carriers, APOE ε4 carriers had lower Aβ42/Aβ40 and greater longitudinal increases in p-tau181 and GFAP; in contrast, the AD-PRS (excluding the APOE region) was associated with greater declines in Aβ42/Aβ40 among APOE ε4 non-carriers. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We detected a significant correlation between AßX-42/X-40 in plasma and CSF (r = 0.473). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers of Alzheimer disease (AD) may facilitate testing of historically under-represented groups. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Levels of CSF Aβ42 decreased in patients with BD who had an episode during follow-up (BD-E) (N = 22) compared to patients without an episode (BD-NE) (N = 25) during follow-up (P = 0.002). 5 key findings →
Design: case-control study Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There were no associations among steps or TRIMP with plasma biomarkers or cognition. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In multivariable analyses, none of the plasma biomarkers were significantly associated with cognitive impairment. 5 key findings →
Participants: 403 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma Aβ42/Aβ40 demonstrated the highest association for Aβ accumulation in the brain with an AUC 0.76 (95%CI = 0.69, 0.82) at C2 N and 0.80 (95%CI = 0.75, 0.86) at Shimadzu. 5 key findings →
Design: cross-sectional Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau (p-tau) biomarkers offer a minimally invasive alternative for detecting Alzheimer’s disease (AD) pathology. 2 key findings →
Participants: 494 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Anti-amyloid treatments for early symptomatic Alzheimer disease have recently become clinically available in some countries, which has greatly increased the need for biomarker confirmation of amyloid pathology. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217 and p-tau217/Aβ42 concentrations demonstrated robust diagnostic performance in a heterogeneous clinical cohort; interpretation requires consideration of kidney function. 5 key findings →
Design: cross-sectional Participants: 509 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma Aβ42/Aβ40, especially when combined with age and APOE ε4 status, accurately diagnoses brain amyloidosis and can be used to screen cognitively normal individuals for brain amyloidosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of 40 included participants (mean [SD] age at death, 88 [8] years; 21 [52%] male), 19 had early-stage dementia with Braak stages III to IV, 13 had resilient brains with similar Braak stages III to IV, and 8 had no dementia (Braak stages 0-II). 4 key findings →
Design: cross-sectional Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The data set included 18 178 patients, of which 10 991 (60.5%) had MCI and 7187 (39.5%) had dementia (mean [SD] age, 75.8 [6.3] years; 9333 women [51.3%]). 3 key findings →
Design: cross-sectional Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this cross-sectional study of plasma biomarkers by race and genetic ancestry, the results indicated that plasma p-tau181, Aβ40, and NFL were lower in African American individuals based on self-reported race but not genetic ancestry. 3 key findings →
Design: cross-sectional Participants: 617 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Due to trisomy of chromosome 21 and the resultant extra copy of the amyloid precursor protein gene, nearly all adults with Down syndrome develop Alzheimer's disease pathology by the age of 40 years and are at high risk for dementia given their increased life expectancy compared with adults with Down syndrome in the past. 1 key finding →
Design: cross-sectional Participants: 41 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of the reference regions used, subcortical white matter, cerebellar white matter, and the pons, alone or in combination, generated the largest effect sizes. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Although recent studies have demonstrated the prognostic utility of plasma biomarkers of Alzheimer pathology or neurodegeneration, such as pTau-181 and NF-L, whether other plasma biomarkers can further improve prediction of cognitive decline is undetermined. 5 key findings →
Design: cohort study Participants: 60 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →