28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
We systematically searched PubMed for eligible studies reporting data on CSF biomarkers reflecting amyloid precursor protein metabolism (Aβ42, Aβ40), neurodegeneration (t-tau), and tangle pathology (p-tau) in symptomatic sporadic CAA cohorts vs controls and patients with Alzheimer disease (AD). 4 key findings →
Design: meta-analysis Participants: 59 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
TREM2 is a transmembrane receptor that is predominantly expressed by microglia in the central nervous system. 4 key findings →
Design: cross-sectional Participants: 1,027 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Increasing evidence suggests an important role of liver function in the pathophysiology of Alzheimer disease (AD). 4 key findings →
Design: cohort study Participants: 1,581 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There is a clear need to characterize and validate molecular biomarkers of cerebral amyloid angiopathy (CAA), in an effort to improve diagnostics, especially in the context of patients with Alzheimer disease (AD) receiving immunotherapies (for whom underlying CAA is the driver of amyloid-related imaging abnormalities). 4 key findings →
Design: meta-analysis Participants: 289 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Peripheral glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are sensitive markers of neuroinflammation and neuronal damage. 4 key findings →
Design: cohort study Participants: 48,542 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this study involving Chinese participants during the 20 years preceding clinical diagnosis of sporadic Alzheimer's disease, we observed the time courses of CSF biomarkers, the times before diagnosis at which they diverged from the biomarkers from a matched group of participants who remained cognitively normal, and the temporal order in which the biomarkers became abnormal. 2 key findings →
Design: case-control study Participants: 648 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 showed larger fold-changes and better accuracy for detecting AD pathology in symptomatic individuals, with greater cross-platform agreement than other p-tau variants. 2 key findings →
Design: case-control study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Aβ-PET was abnormal in 81 participants from J-TRC and 71 participants from BioFINDER. 2 key findings →
Design: cross-sectional Participants: 474 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The primary constituents of plaques (Aβ42/Aβ40) and neurofibrillary tangles (tau and phosphorylated forms of tau [ptau]) are the current leading diagnostic and prognostic cerebrospinal fluid (CSF) biomarkers for AD. 3 key findings →
Design: case-control study Participants: 5,161 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Overall the study included 199 participants with iRBD, 20 hyposmic participants with available dopamine transporter single-photon emission computed tomography, 146 nonmanifest GBA1N409S gene carriers, 21 GBA1N409S gene carrier patients with PD, 50 patients with sporadic PD, and 140 healthy controls. 3 key findings →
Design: cross-sectional Participants: 170 Evidence: low
Full summary, score breakdown and related studies → Original source
We demonstrated that peripherin is distributed in sciatic nerve, and to a lesser extent spinal cord tissue lysates, but not in brain or extra-neural tissues. 3 key findings →
Design: longitudinal study Participants: 45 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 may capture earlier Alzheimer's disease (AD)-related cognitive and brain atrophy hallmarks in females compared to males, possibly reflective of increased susceptibility to AD pathophysiology. 2 key findings →
Design: longitudinal study Participants: 163 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results encourage an independent validation cohort study to confirm the indication that the plasma Aβ 1-40 /Aβ 1-42 ratio, assessed via Simoa, may improve future standard of care and clinical trial design. 2 key findings →
Design: cohort study Participants: 276 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This represents the largest U.S.-based, multi-site, biomarker initiative of AD in DS. 1 key finding →
Design: longitudinal study Participants: 400 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our review summarizes the diagnostic accuracy of plasma and cerebrospinal fluid (CSF) phosphorylated tau 217 (p-tau217) in detecting amyloid and tau pathology on positron emission tomography (PET). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The mitochondrial cascade hypothesis of Alzheimer's disease (AD) has been portrayed through molecular, cellular, and animal studies; however large epidemiological studies are lacking. 3 key findings →
Design: cohort study Participants: 790 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neurofilament light (NFL) is a putative biomarker of neurodegeneration. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
P-tau/Aβ42 is sufficient for predicting progression in AD, with very high accuracy. 1 key finding →
Design: longitudinal study Participants: 1,983 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings suggest that plasma pTau181 is a promising biomarker for concurrent ADNC and amyloidosis in LBD. 3 key findings →
Design: longitudinal study Participants: 565 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 428 participants were included; 167 had normal cognition, 245 had MCI, and 16 had mild AD. 2 key findings →
Design: cross-sectional Participants: 428 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These results suggested that distinct meta-cognitive profiles can be identified in preclinical-AD. 5 key findings →
Design: cohort study Participants: 314 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The available evidence suggests that ethnicity and race may influence blood biomarker concentrations. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
This Swedish study of over 1,200 people with memory symptoms found that a blood test combining p-tau217 with an amyloid ratio (the 'Amyloid Probability Score 2') was far more accurate at identifying Alzheimer's disease than doctors' clinical judgment alone. 3 key findings →
Design: cross-sectional Participants: 1,213 Evidence: high
Full summary, score breakdown and related studies → Original source
This large multi-country study tested a fully automated, commercially available blood test (Lumipulse platform, measuring p-tau217) in nearly 1,800 people across memory clinics and, notably, primary care doctors' offices in Sweden, Spain, and Italy. 5 key findings →
Design: cross-sectional Participants: 1,767 Evidence: high
Full summary, score breakdown and related studies → Original source
In a Chinese cohort of 1,275 people spanning normal cognition to dementia, this study compared three blood markers: p-tau217 rose steadily as amyloid and tau pathology worsened and was very good at both ruling out early disease and flagging advanced tau pathology. 4 key findings →
Design: cohort Participants: 1,275 Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 3,322 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 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 →