27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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Trisomy 21 or Down syndrome (DS) is the most frequent genetic cause of mental retardation, affecting one in 800 live born human beings. 1 key finding →
Evidence: low
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In a longitudinal study in which all participants were healthy at the time of their entry into the study, the present authors compared the amount of decline on the subtests of the WISC-R to determine the sequence of cognitive decline associated with varying stages of dementia. 5 key findings →
Design: longitudinal study Participants: 44 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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This first evaluation of 18 F-MK6240 in DS demonstrates its suitability as a sensitive biomarker for Alzheimer's disease tau pathology. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
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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Individuals with DS have a substantially increased risk of mortality due to specific causes and may have an elevated risk of other incident cancers in addition to leukemia. 4 key findings →
Participants: 22 Evidence: moderate
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In the United States, estimates indicate there are between 250,000 and 400,000 individuals with Down syndrome (DS), and nearly all will develop Alzheimer's disease (AD) pathology starting in their 30s. With the current lifespan being 55 to 60 years, approximately 70% will develop dementia, and if their life expectancy continues to increase, the number of individuals developing AD will concomitantly increase. 4 key findings →
Participants: 400,000 Evidence: low
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At present, there may be over 210,000 people with Down syndrome (DS) over the age of 55 in the United States (US) who have significant needs for augmented services due to circumstances related to ordinary and/or pathological aging. 1 key finding →
Participants: 210,000 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
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The activity of the pyruvate dehydrogenase complex (PDHC) was reduced in affected areas of brain from patients with Huntington disease (caudate, putamen) and Alzheimer disease (frontal cortex) where choline acetyltransferase (CAT) activity was low. 1 key finding →
Evidence: low
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We propose the following sequence of events in the development of neuropathologic changes of Alzheimer disease in Down syndrome: (1) intracellular accumulation of Abeta in neurons and astrocytes, (2) deposition of extracellular Abeta and formation of diffuse plaques, and (3) development of neuritic plaques and neurofibrillary tangles with activation of microglial cells. 1 key finding →
Participants: 14 Evidence: low
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Down syndrome (also known as trisomy 21) is the model human phenotype for all genomic gain dosage imbalances, including microduplications. 4 key findings →
Evidence: low
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Alzheimer disease (AD) represents an oncoming epidemic that without an effective treatment promises to exact extraordinary human and financial burdens. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In patients with Down syndrome, senile plaques and neurofibrillary tangles accumulate in the cortex at an earlier age than in persons of normal karyotype. 5 key findings →
Participants: 20 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 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 →