27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
In Down syndrome, enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic early mental retardation and precocious neurodegeneration of Alzheimer type. 2 key findings →
Evidence: low
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Serum tests of thyroid function were compared in Down syndrome (DS) patients with and without manifestations of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Down syndrome is caused by trisomy of chromosome 21 and is comprised of a constellation of abnormalities including neuropathological features that closely resemble those characterizing the neurodegeneration of Alzheimer disease. 1 key finding →
Evidence: low
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Growth inhibitory factor, a new metallothioneinlike protein, was investigated at postmortem examination in the brains of 18 patients with Down syndrome ranging in age from 18 weeks gestation to 50 years of age and in 20 age-matched normal controls by developmental immunohistochemistry. 5 key findings →
Participants: 18 Evidence: low
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Postmortem morphometric analyses of Bielschowsky stained sections from brains of 70 mentally retarded people without Down syndrome, age 65 and over when they died, indicated Alzheimer-type neuropathology in 22 cases (31%) and a majority with at least presence of some Alzheimer-type lesions. 4 key findings →
Participants: 25 Evidence: low
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Previous research has revealed similarities in the neuropathology, clinical presentation, and risk factors between persons with Alzheimer disease from the general population (GP-AD) and those with Down syndrome (DS-AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In order to study whether phosphokinases might be involved in the neuropathology of Down Syndrome (DS) and Alzheimer disease (AD), cyclin dependent kinase (CDK) activity and protein, phosphokinase C (PKC) and phosphokinase A (PKA) activities have been determined in frontal lobes of DS, AD and control brains. 1 key finding →
Evidence: low
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Cognitive profiles of performances were obtained from a selected group of adult Down syndrome (DS) subjects (n = 20; mean age: 34.5 years; s.d.: 7.7) by means of an ad hoc neuropsychological battery. 3 key findings →
Participants: 20 Evidence: low
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Genome-wide deregulation contributes to mitochondrial dysfunction and impairment in oxidative phosphorylation (OXPHOS) mechanism resulting in oxidative stress, increased production of reactive oxygen species (ROS) and cell death in individuals with Down syndrome (DS). 1 key finding →
Evidence: low
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Evolutionary aspects of menopause are considered from several perspectives. 1 key finding →
Evidence: low
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Myoclonic epilepsy is being increasingly recognized as a late-onset complication in middle-aged or elderly patients with Down syndrome, in association with cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apoptosis is the mechanism by which cells are programmed to die under a wide range of physiological and developmental stimuli. 3 key findings →
Evidence: low
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Magnetic resonance imaging is potentially a valuable tool in the diagnosis of Alzheimer disease in adults with Down syndrome, particularly in individuals for whom standard intellectual assessments are not possible. 2 key findings →
Evidence: low
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IgG subclasses were measured in sera from 33 persons with Down syndrome (DS) (mean age 55 +/- 7 years) and 33 age- and sex-matched control individuals using a mouse monoclonal antibody based sandwich enzyme linked immunosorbent assay. 3 key findings →
Participants: 33 Evidence: low
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The identified deficits in the medical care of the target population and the approaches to solving them will be incorporated into the development of health policy recommendations in order to optimize the care situation of those affected in the long term. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is the most common genetic cause of intellectual impairment, characterised by an extra copy of chromosome 21. 5 key findings →
Evidence: low
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We observed higher within‐ and between‐DMN FC in the CS‐OSA compared to the CI‐OSA group; however, this difference was not observed between the CS‐nonOSA and CI‐nonOSA groups. 5 key findings →
Evidence: low
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Down syndrome (DS) patients suffer from mental retardation, but also display enhanced beta-APP production and develop cortical amyloid plaques at an early age. 3 key findings →
Evidence: low
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In past decades, most individuals with Down syndrome were usually not afforded adequate medical care. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Because of their initially low levels of mental functioning, Down syndrome persons' clinical symptoms frequently go undetected until the disease is advanced and deterioration severe. 1 key finding →
Evidence: low
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Early-onset cataract and Alzheimer's disease occur with high frequency in Down syndrome (trisomy 21), the most common chromosome duplication in human live births. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Human carbonyl reductase (CBR) belongs to a group of NADPH-dependent enzymes called aldo-keto reductases. 1 key finding →
Evidence: low
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We previously observed low level mosaicism (2-4% normal cells) in phytohemagglutinin-stimulated peripheral blood lymphocytes (PBL) in 29% of a small group of elderly persons with Down syndrome (DS). 3 key findings →
Evidence: low
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The decrease in the number of neurons free of neurofibrillary changes, neurons with neurofibrillary degeneration, and the total volume of beta-amyloid (A beta) deposits in the amygdala of people with Down syndrome and in late stages of Alzheimer disease were estimated by using morphometry and regression analysis. 3 key findings →
Evidence: low
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The cause(s) of Alzheimer disease (AD) remain unknown. 5 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 536 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →