29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Trisomy 21, the presence of a supernumerary chromosome 21, results in a collection of clinical features commonly known as Down syndrome (DS). 1 key finding →
Evidence: low
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We have purified and characterized the cerebral amyloid protein that forms the plaque core in Alzheimer disease and in aged individuals with Down syndrome. 5 key findings →
Evidence: low
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This exploratory case-control study investigates the synaptic marker beta-synuclein in serum and plasma pTau181 in adults with Down syndrome (DS) with (sDS, n = 14) and without (aDS, n = 47) clinical symptoms of Alzheimer disease (AD) as well as euploid controls (n = 23). 1 key finding →
Design: case-control study Participants: 14 Evidence: moderate
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For both cohorts, the prevalence of mosaicism was 40 and Aβ 42 concentrations. 2 key findings →
Design: longitudinal study Participants: 357 Evidence: moderate
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Of 115 participants (mean age 40.0 ± 9.2 years; 43.5% female), higher interdaily stability was associated with higher DSMSE scores B = 20.6 (95% CI 5.0-36.2). 4 key findings →
Design: cross-sectional Participants: 115 Evidence: low
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Individuals with DS were more likely to have microbleeds than controls (20% vs 8.9%, p 60 years) and AD clinical stage (12.42% asymptomatic, 27.9% prodromal, 35.09% dementia) were more common in APOE ε4 carriers (26% vs 18.3% noncarriers, p = 0.008), but not associated with vascular risk factors ( p > 0.05). 4 key findings →
Design: cross-sectional Participants: 276 Evidence: low
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Establishing this clinical definition supports future research and investigation of an underlying mechanism. 1 key finding →
Design: case-control study Participants: 35 Evidence: moderate
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Down syndrome (DS) is the most common condition with intellectual disability and is caused by trisomy of Homo sapiens chromosome 21 (HSA21). 2 key findings →
Design: longitudinal study Evidence: moderate
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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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Individuals with Down syndrome (DS) have a genetically determined form of Alzheimer's disease (AD) due to the amyloid precursor protein (APP) gene dose effect. 1 key finding →
Design: longitudinal study Evidence: moderate
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Among adults with DS, decreasing levels of plasma Aβ42, a decline in the Aβ42/Aβ40 ratio, or increasing levels of Aβ40 may be sensitive indicators of conversion to AD, possibly reflecting compartmentalization of Aβ peptides in the brain. 3 key findings →
Participants: 225 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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A population of more than six million people worldwide at high risk of Alzheimer's disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 1 key finding →
Evidence: low
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Adults with DS have a significantly increased brain concentration of myo-inositol, and this is associated with reduced cognitive ability. 5 key findings →
Design: case-control study Participants: 38 Evidence: moderate
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Compared to controls, mean CSF NPTX2 levels were lower in DS at all AD stages; aDS (0.6-fold, adj.p 0.07). 2 key findings →
Design: cross-sectional Participants: 49 Evidence: low
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To determine if proton magnetic resonance spectroscopy ((1)H-MRS) detect differences in dementia status in adults with Down syndrome (DS), we used (1)H-MRS to measure neuronal and glial metabolites in the posterior cingulate cortex in 22 adults with DS and in 15 age- and gender-matched healthy controls. 5 key findings →
Design: longitudinal study Participants: 22 Evidence: moderate
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These findings suggest significant binding of lecanemab to cerebral amyloid angiopathy in DS. 5 key findings →
Participants: 15 Evidence: moderate
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Epilepsy was associated with higher subsequent recording of dementia and mortality over 2 years. 4 key findings →
Design: cohort study Participants: 1,812 Evidence: moderate
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These findings emphasize the necessity of tailoring mAb trials for DS, considering age-related AD characteristics. 5 key findings →
Design: cross-sectional Evidence: low
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Endocytosis is critical to the function and fate of molecules important to Alzheimer's disease (AD) etiology, including the beta protein precursor (betaPP), amyloid beta (Abeta) peptide, and apolipoprotein E (ApoE). 3 key findings →
Evidence: low
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Down syndrome, which arises in individuals carrying an extra copy of chromosome 21, is associated with a greatly increased risk of early-onset Alzheimer disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Geroscience, the new interdisciplinary field that aims to understand the relationship between aging and chronic age-related diseases (ARDs) and geriatric syndromes (GSs), is based on epidemiological evidence and experimental data that aging is the major risk factor for such pathologies and assumes that aging and ARDs/GSs share a common set of basic biological mechanisms. 2 key findings →
Evidence: low
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Down syndrome (DS) is a major cause of mental retardation and congenital heart disease. 2 key findings →
Evidence: low
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Synapses are essential components of neurons and allow information to travel coordinately throughout the nervous system to adjust behavior to environmental stimuli and to control body functions, memories, and emotions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
People with Down syndrome (DS) are at high risk for developing Alzheimer disease (AD) with age. 2 key findings →
Participants: 32 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.
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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →