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
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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
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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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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
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Between Feb 1, 2013, and June 28, 2019 (Barcelona), and between June 1, 2009, and Dec 31, 2014 (Cambridge), we included 388 participants with Down syndrome (257 [66%] asymptomatic, 48 [12%] with prodromal Alzheimer's disease, and 83 [21%] with Alzheimer's disease dementia) and 242 euploid controls.
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Inter-rater agreement for ID level classification was 95% within sites but 60% between sites. 5 key findings →
Design: cohort study Participants: 673 Evidence: moderate
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Plasma p-tau212 might have utility for theragnostics, monitoring therapy efficacy, and as a target engagement biomarker in clinical trials both in sporadic and DSAD. 1 key finding →
Participants: 245 Evidence: low
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Almost all individuals with Down Syndrome (DS) develop Alzheimer's disease (AD) by mid to late life. 3 key findings →
Participants: 229 Evidence: moderate
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These findings highlight LBP prevalence in DSAD but suggest current SAA may fail to detect limited αSyn deposition. 4 key findings →
Participants: 270 Evidence: moderate
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Diagnosing Alzheimer's disease (AD) in adults with Down syndrome (DS), a population with a high genetically determined risk of AD, remains challenging. 1 key finding →
Participants: 2,329 Evidence: low
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Magnetic resonance spectroscopy detects Alzheimer's disease related inflammation and neurodegeneration, and could be a good noninvasive disease-stage biomarker in Down syndrome. 3 key findings →
Participants: 118 Evidence: moderate
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The DABNI cohort included 1,135 participants with a mean age of 42.82 years (SD = 11.56), 46.3% of whom are female. 5 key findings →
Design: longitudinal study Participants: 1,135 Evidence: moderate
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There is a need for early, objective markers of Alzheimer's disease (AD)-related synapse dysfunction in adults with Down syndrome (DS). 1 key finding →
Design: cross-sectional Participants: 131 Evidence: moderate
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Novel insights into Alzheimer's disease through the study of individuals with Down syndromePeople with Down syndrome (DS) represent the largest genetically defined population at risk for Alzheimer's disease (AD). 1 Virtually all adults with DS develop AD neuropathology by midlife due to triplication of the amyloid precursor protein (APP) gene on chromosome 21.As medical advances and social integration have extended life expectancy into the 60s, AD has emerged as the major determinant of cognitive decline, morbidity, and mortality in this DS population. 2 What was once viewed as an inevitable consequence of aging in DS is now recognized as a unique scientific opportunity to uncover the earliest events that drive AD.The predictable and accelerated course of DS-associated AD (DSAD) provides an unparalleled window into the molecular and cellular origins of amyloid and tau pathology, neuroinflammation, cerebrovascular pathology, and neurodegeneration. 1 key finding →
Design: longitudinal study Evidence: moderate
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There is an urgent need for objective markers of Alzheimer's disease (AD)-related cognitive impairment in people with Down syndrome (DS) to improve diagnosis, monitor disease progression, and assess response to disease-modifying therapies. 1 key finding →
Participants: 80 Evidence: moderate
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LP can be safely performed to study CSF biomarkers in DS. 1 key finding →
Participants: 80 Evidence: low
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The brain metabolic decline in DS with age reflects Alzheimer's pathological processes and involves temporoparietal regions in a similar pattern to that found in other forms of AD. 4 key findings →
Participants: 71 Evidence: low
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This well-characterized case of PCA syndrome due to AD in a very young patient with DS demonstrates the occurrence of atypical presentations in DS that might be overshadowed by the baseline intellectual disability associated with DS. 5 key findings →
Evidence: low
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BackgroundMost adults with Down syndrome will develop Alzheimer's disease (AD) due to the triplication of the amyloid precursor protein in the 21 st chromosome. 1 key finding →
Design: case-control study Evidence: moderate
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Down syndrome (DS) is a complex genetic condition due to an additional copy of human chromosome 21, which results in the deregulation of many genes. 5 key findings →
Design: cross-sectional Evidence: low
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Down syndrome (DS) is the main genetic cause of intellectual disability worldwide. 3 key findings →
Evidence: low
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PSMD was more strongly associated with age in DS (rho=0.56; p <0.001) than in HC (rho=0.38, p <0.001; Figure 1A), with regression lines starting to diverge at age 42. 5 key findings →
Design: cross-sectional Participants: 70 Evidence: low
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There is an urgent need for objective markers of Alzheimer’s disease (AD)-related cognitive impairment in people with Down syndrome (DS) to improve diagnosis, monitor disease progression and assess response to disease-modifying therapies. 4 key findings →
Participants: 80 Evidence: moderate
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In DS, PSMD changed approximately 10‐15 years before the onset of AD symptoms and linearly increased with AD clinical stages, AD pathology, and SVD metrics. 4 key findings →
Participants: 70 Evidence: low
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Amyloid pathology in aDS individuals is linked to frontal‐predominant atrophy without clear hypometabolism. 5 key findings →
Participants: 29 Evidence: low
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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 →