27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The variability in disease onset was compared with that of autosomal dominant Alzheimer disease. 5 key findings →
Design: meta-analysis Participants: 77 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In general linear models lower plasma Aβ42/40 was related to lower visuospatial ability, higher total tau was related to lower episodic memory, and higher NfL was related to lower visuospatial ability and lower episodic memory. 3 key findings →
Design: cohort study Participants: 260 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Dementia was associated with mortality in 70% of older adults with DS. 5 key findings →
Design: longitudinal study Participants: 300 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →
Design: cohort study Participants: 137 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is a genetic form of Alzheimer's disease (AD) that offers crucial insights into AD pathogenesis. 2 key findings →
Design: cohort study Participants: 1,135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer's disease. 5 key findings →
Design: longitudinal study Participants: 132 Evidence: moderate
Full summary, score breakdown and related studies → Original source
At baseline, there were 436 asymptomatic individuals, 69 patients with prodromal AD, and 127 with AD dementia. 2 key findings →
Design: cohort study Participants: 632 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There were 132 720 unique adults with Down syndrome from 2011 to 2019: 79 578 (53.2%) were male, 17 090 (11.7%) were non-Hispanic Black, 20 777 (15.7%) were Hispanic, 101 120 (68.8%) were non-Hispanic White, and 47 692 (23.3%) had ever had an Alzheimer dementia diagnosis. 3 key findings →
Design: cohort study Participants: 132 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
High levels of Aβ42 and tau in both young controls and DS suggest these proteins are produced by normal physiological processes, whereas the changes seen in later life are consistent with emergence of pathological alterations. 4 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The diagnostic performance of plasma biomarkers was poor (area under the curve [AUC] between 0·53 [95% CI 0·44-0·62] and 0·74 [0·66-0·82]) except for plasma NfL concentrations, which had an AUC of 0·88 (0·82-0·93) for the differentiation of the asymptomatic group versus the prodromal Alzheimer's disease group and 0·95 (0·92-0·98) for the asymptomatic group versus the Alzheimer's disease dementia group. 4 key findings →
Design: cross-sectional Participants: 282 Evidence: low
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Among 300 participants with DS and a control group of 37 non-DS siblings, mean (SD) age was 45.0 (10.1) years, and 167 (49.6%) were men. 4 key findings →
Design: cross-sectional Participants: 300 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with Down syndrome over age 40 years are at risk for developing dementia of the Alzheimer type and have evidence for chronic oxidative stress. 4 key findings →
Participants: 53 Evidence: high
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Adults with Down syndrome demonstrate striatum-first amyloid accumulation with [ 11 C]PiB PET imaging, which has not been replicated with [ 18 F]florbetapir (FBP). 4 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
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
Reduced exposure to environmental factors that contribute to cancer risk, tumour-suppressor genes on chromosome 21, or a slower rate of replication or higher likelihood of apoptosis in Down's syndrome cells, could be possible reasons for paucity of cancer in people with Down's syndrome. 4 key findings →
Participants: 17,897 Evidence: low
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Clinical and neuropathologic evidence points to the development of Alzheimer's disease (AD) in seven Down's syndrome patients above age 40. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Older Medicare beneficiaries in California with DS, especially those with dementia, have a high level of multimorbidity including several treatable conditions. 3 key findings →
Design: cross-sectional Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Global PET amyloid burden was compared with regards to cognitive status, APOE ɛ4 status, sex, age, and estimated years to symptom onset. 2 key findings →
Design: cross-sectional Participants: 216 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Virtually all adults with Down syndrome (DS) show the neuropathological changes of Alzheimer disease (AD) by the age of 40 years. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among adults with Down syndrome, the striatum consistently accumulates amyloid earlier than the cortex when measured with PiB. 2 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Aβ40 levels changed less for the simvastatin group (not statistically significant). 4 key findings →
Design: cohort study Participants: 21 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
NF-L is a biomarker for neurodegeneration in DS with potential for use in future clinical trials to prevent or delay dementia. 2 key findings →
Design: cross-sectional Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Adults with Down syndrome develop the neuropathological hallmarks of Alzheimer's disease and are at very high risk of developing early-onset dementia, which is now the leading cause of death in this population. 1 key finding →
Evidence: low
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 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 →