28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
We used within-group locally estimated scatterplot smoothing models to compare the trajectory of biomarker changes with age in females versus males, as well as by apolipoprotein ɛ4 carriership. 5 key findings →
Design: cross-sectional Participants: 628 Evidence: low
Full summary, score breakdown and related studies → Original source
Animal studies show aging varies between individuals as well as between organs within an individual 1-4 , but whether this is true in humans and its effect on age-related diseases is unknown. 5 key findings →
Participants: 5,676 Evidence: low
Full summary, score breakdown and related studies → Original source
GFAP was associated with amyloid and tau PET in multivariable models. 4 key findings →
Design: cross-sectional Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma Aβ42/40 was a robust biomarker for AD which was not affected by renal function. 5 key findings →
Design: cross-sectional Participants: 645 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a common neurodegenerative disease characterized by amyloid plaques and impaired brain metabolism. 4 key findings →
Design: cross-sectional Participants: 181 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These results suggest that prevalence of brain amyloid pathology differed, but that eligibility based on plasma was equally effective across racial and ethnic group members. 3 key findings →
Participants: 4,905 Evidence: low
Full summary, score breakdown and related studies → Original source
One hundred forty-six subjects (56 probable MCI-LB, 22 possible MCI-LB, 44 MCI-AD, and 24 controls) were reviewed for up to 5.7 years. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
After the clinical implementation of amyloid-β-targeting therapies for people with cognitive impairment due to Alzheimer's disease (AD), there is an urgent need to efficiently identify this patient population in primary care. 4 key findings →
Participants: 223 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Global implementation of blood tests for Alzheimer's disease (AD) would be facilitated by easily scalable, cost-effective and accurate tests. 4 key findings →
Participants: 337 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These analyses provide preliminary support for IICV as a marker of incident AD and MCI. 4 key findings →
Design: longitudinal study Participants: 105 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Most investigations have previously focused on highly selected cohorts with established AD-endophenotypes (CSF biomarkers, autopsy report, PET etc.), while data on cohorts with clinical assessment are currently lacking, especially in non-European populations. 2 key findings →
Participants: 234 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We investigated plasma phosphorylated tau217 (p-tau217) and p-tau181 efficacy in predicting positive amyloid positron emission tomography (PET) results and cognitive stage transitions. 2 key findings →
Participants: 121 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is characterized by cognitive impairments that hinder daily activities and lead to personal and behavioral problems. 3 key findings →
Design: prospective cohort Participants: 41 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The assessment of serum NfL and p-Tau 181 may provide a comprehensive view of FTLD, aiding in the differential diagnosis, in staging disease severity and in defining survival probability. 2 key findings →
Design: cross-sectional Participants: 417 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Inner retina in Alzheimer's Disease (AD) may experience neuroinflammation resulting in atrophy. 3 key findings →
Design: case-control study Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) neurofilament light (NFL) is a marker of axonal degeneration. 2 key findings →
Design: longitudinal study Participants: 144 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers of AD/ADRD are influenced by common demographic and clinical characteristics. 2 key findings →
Participants: 779 Evidence: high
Full summary, score breakdown and related studies → Original source
After adjusting for age, sex, and the apolipoprotein E ( APOE ) alleles, compared to the CN group, the plasma t-tau, and NfL were significantly increased in the AD group ( p < 0.01, Bonferroni correction). 4 key findings →
Design: cross-sectional Participants: 277 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results show that the measurement of p-Tau181 in plasma has great potential as a non-invasive prognostic screening tool for implementation in a clinical setting. 5 key findings →
Participants: 138 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings indicate that the high plasma AβO level could serve as a potential surrogate biomarker of severe SCD and the presence of brain Aβ deposition in individuals with normal objective cognition. 5 key findings →
Design: cross-sectional Participants: 126 Evidence: low
Full summary, score breakdown and related studies → Original source
Early diagnosis of Alzheimer's disease (AD) is a crucial starting point in disease management. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Researchers at the University of Pittsburgh developed a new plasma p-tau217 test (using a different antibody than existing commercial tests) and validated it in 363 people, including some with genetic early-onset Alzheimer's mutations and community-dwelling older adults. 4 key findings →
Design: cross-sectional Participants: 363 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF biomarkers, including P-tau, T-tau, Aβ 42 , Aβ 40 , and NFL, support in vivo identification of AD neuropathology and correlate with FTLD neuropathology. 4 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The combination of sAPPβ with YKL-40 and with NfL in CSF could be useful to increase the certainty of the diagnosis of FTLD-related syndromes in clinical practice. 2 key findings →
Design: cross-sectional Participants: 159 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Although all p-tau variants increased across the AD continuum, p-tau217 Lilly showed the greatest dynamic range (13-fold increase vs 1.9-5.4-fold increase for other p-tau variants for AD dementia vs non-AD). 2 key findings →
Participants: 334 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
9 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 9. The same 9 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 →