28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma amyloid beta protein 1-40 (Abeta40) and Abeta42 levels were quantitated from 28 young Down syndrome (DS) (20-40 years old), 28 age-matched controls, 32 old DS (41-65 years old) and 32 age-matched controls in a sandwich enzyme-linked immunosorbent assay. 1 key finding →
Evidence: low
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We immunohistochemically studied the expression of beta-amyloid precursor protein (APP), Abeta40, Abeta42, and Abeta43 in the frontal lobes of 20 Down syndrome (DS) patients and 13 controls. 5 key findings →
Evidence: low
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Patients with Down syndrome (DS) over 40 years of age, prematurely and consistently develop neurofibrillary tangles (NFT), intracytoplasmic inclusions of highly insoluble straight or paired helical 12-16 nm filaments, and senile plaques (SP) composed of abnormal neurites surrounding a core of beta amyloid. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The association of generalized epilepsy with elderly DS represents an epiphenomenon in evolution which is associated with a progressive deterioration of cognitive and motor functions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest that, with respect to this putative marker of central cholinergic activity, dementia in aging DS shares pathophysiological similarities to AD in the general population. 2 key findings →
Participants: 12 Evidence: low
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The cognitive deficits in Down syndrome (DS) are attributed to an excessive hippocampal inhibition, which obstructs neuronal plasticity and normal learning and memory, a view which is largely based on studies of Ts65Dn mice, the best characterized mouse model of DS. 1 key finding →
Evidence: low
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Individual differences in the development of neurofibrillary changes were examined in eight cortical regions in the brains of 43 subjects with Down syndrome (DS; age range, 15-69 years) using sections stained with monoclonal antibodies (mAb) tau-1 and 3-39. 2 key findings →
Participants: 43 Evidence: low
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Thyroid hormone abnormalities are strongly associated with Down Syndrome (DS) with elevated thyroid stimulating hormone (TSH) levels as the most consistent finding. 4 key findings →
Evidence: low
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Trisomy 21 (Down syndrome, DS) is the most common genetic cause of mental retardation, resulting from triplication of the whole or distal part of human chromosome 21. 2 key findings →
Evidence: low
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The presenilin-1 (PS1) gene mutation (Pro117Leu), recently identified in a Polish family is characterized by the earliest reported onset (from 24-31 years) of Alzheimer disease (AD) and a very short duration of disease (4-6 years). 3 key findings →
Evidence: low
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Frequencies of chromatid aberrations in response to G2-phase x-irradiation were compared in PHA-stimulated blood lymphocytes from healthy control subjects, Down syndrome (DS) patients, and Alzheimer disease (AD) patients. 4 key findings →
Evidence: low
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Alzheimer's disease is a neurodegenerative disorder characterized by global cognitive decline. 1 key finding →
Evidence: low
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This study supports the need for formal reliability and validity studies of TM preparatory to the consideration of this modality for use in clinical trials for AD. 1 key finding →
Participants: 90 Evidence: low
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We evaluated the allele (and genotype frequencies in 60 Down syndrome (DS), 25 mothers and 57 controls from Sicily and its relation with mental retardation. 2 key findings →
Evidence: low
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Thirty-four years ago, amyloid-β 1-42 peptide was identified in amyloid plaques from brain tissue obtained from patients with Alzheimer disease (AD) and Down syndrome. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Due to a triplication of the amyloid precursor protein (APP) gene on chromosome 21, most people with Down's Syndrome (DS) are at high risk of developing an Alzheimer type of dementia associated with Down's Syndrome (DS-AD). 1 key finding →
Evidence: low
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Down syndrome (DS), caused by trisomy of chromosome 21 (HSA21), is a complex condition associated with neurodevelopmental impairments and accelerated brain aging, often culminating in early-onset Alzheimer's disease (AD). 1 key finding →
Evidence: low
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In the last decade, a number of important research advances in different fields have allowed Down syndrome (DS) research to flourish, creating a time of both unparalleled opportunity and considerable challenge. 1 key finding →
Evidence: low
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Patients with Alzheimer disease (AD) show visual impairments in color discrimination (blue hues), stereoacuity, and contrast sensitivity. 3 key findings →
Participants: 22 Evidence: low
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SET is a multifunctional protein, but when present in the cytoplasm, acts as a powerful inhibitor of phosphatase 2A. We previously observed that in CA1 of Down syndrome (DS) patients, the level of SET is increased, and SET is translocated to the cytoplasm and associated with the hyperphosphorylation of tau at ser202/thr205. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The dementia of Alzheimer disease (AD) correlates with the deposition of extracellular amyloid, and this amyloid arises from the abnormal processing of a high molecular weight amyloid peptide precursor (APP), which is a normal cellular protein that is found in both brain and in peripheral tissues in humans. 1 key finding →
Participants: 25 Evidence: low
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Studies in the neurotypical population have demonstrated that personal social networks can mitigate cognitive decline and the development of Alzheimer disease. 2 key findings →
Evidence: low
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Lysosome dysfunction arises early and propels Alzheimer’s Disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with characteristic neuropathological changes of the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial stress is one of the early features of Alzheimer disease (AD). 4 key findings →
Evidence: low
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →