30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our results confirm that PM20D1 is an mQTL in AD and demonstrate that it plays a dynamic role at different stages of the disease. 3 key findings →
Design: longitudinal study Participants: 649 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study found that boys with the PSEN1 variant had decreased working memory abilities compared with girls with the variant and boys and girls without the variant, suggesting a sex-specific genetic risk in early life cognitive performance among individuals with the PSEN1 variant. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum NfL concentration is increased in FAD prior to symptom onset and correlates with measures of disease stage and severity. 3 key findings →
Design: cross-sectional Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
While APOEε4 is associated with increased amyloid-β burden, its association with cerebral tau pathology has been controversial. 5 key findings →
Design: cross-sectional Participants: 124 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Previous studies have suggested that the APOE ɛ4 allele plays a role in the risk and age at onset of dementia in DS; however, data on in vivo biomarkers remain scarce. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Baseline NfL was elevated in symptomatic carriers (median 52 pg/mL [IQR 24-69]) compared with presymptomatic carriers (9 pg/mL [6-13]; p<0·0001) and non-carriers (8 pg/mL [6-11]; p<0·0001), and was higher in converters than in non-converting carriers (19 pg/mL [17-28] vs 8 pg/mL [6-11]; p=0·0007; adjusted for age). 4 key findings →
Design: cohort study Participants: 59 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Panama Aging Research Initiative is a cohort study of 423 adults aged ≥65 years recruited from an outpatient geriatric department of Panama's largest public hospital, the Social Security Fund's Dr Arnulfo Arias Madrid Hospital Complex (Complejo Hospitalario Dr Arnulfo Arias Madrid de la Caja de Seguro Social). 5 key findings →
Design: cohort study Participants: 423 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is evidence that serum NfL is increased more than a decade before the onset of clinical symptoms in FAD and rises thereafter. 3 key findings →
Design: longitudinal study Participants: 61 Evidence: moderate
Full summary, score breakdown and related studies → Original source
MTUS2 encodes a microtubule associated protein implicated in the development and function of the nervous system, making it a plausible candidate to investigate LOAD biology. 4 key findings →
Participants: 14,260 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings support use of U-p53AZ as blood-based biomarker predicting whether individuals would reach neuropsychologically-defined AD within six years prior to AD diagnosis. 5 key findings →
Design: longitudinal study Participants: 482 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Overall, memory worsened from age 30 years through the 90s. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age. 5 key findings →
Design: cross-sectional Participants: 1,246 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We enrolled a cohort of 1070 PSEN1 E280A mutation carriers and 1074 non-carriers with baseline assessments; of these participants, longitudinal measures (with a mean follow-up of 6 years) were available for 242 mutation carriers and 262 non-carriers. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase. 2 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Genome-wide significant loci were identified for all biomarkers, including DACT1-DAAM1 (pTau217), KCNJ3 (pTau181), KLHDC4 (NfL), SLC10A7 (GFAP), and PPP4R2 (composite score). 4 key findings →
Participants: 1,972 Evidence: moderate
Full summary, score breakdown and related studies → Original source
E280A carriers had higher p-tau231 levels than non-carriers (9.0 ± 7.4 vs. 5.2 ± 3.4 pg/mL, P < 0.001). 5 key findings →
Design: longitudinal study Evidence: moderate
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
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
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
NfL in both serum and CSF has the potential to serve as a biomarker for clinical disease onset and has a prognostic value in genetic FTD. 1 key finding →
Design: case-control study Participants: 174 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
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
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
In vitro studies of autosomal dominant Alzheimer's disease implicate longer amyloid-β peptides in disease pathogenesis; however, less is known about the behaviour of these mutations in vivo. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events