27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Declines in adaptive behavior were examined in a study of dementia in adults with Down syndrome and other forms of mental retardation. 2 key findings →
Evidence: low
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Down syndrome remains one of the most common causes of mental retardation. 1 key finding →
Evidence: low
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It has been clearly established that there is an increased incidence of early onset dementia of the Alzheimer type (DAT) in people who have Down syndrome. 5 key findings →
Evidence: low
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In order to study whether Alzheimer-like neuropathological changes involve the central histaminergic system we measured the concentration of histamine, its precursor histidine as well as the activity of histidine decarboxylase (HDC) and histamine-N-methyl-transferase (HMT) in frontal cortex of aging Down syndrome (DS) patients, Alzheimer patients and control individuals. 3 key findings →
Evidence: low
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The activities of red blood cell enzymes that scavenge the superoxide radical and hydrogen peroxide were measured in severely to profoundly retarded adult Down syndrome (DS) patients with and without manifestations of Alzheimer disease (AD), and control individuals matched for sex, age, and time of blood sampling. 4 key findings →
Evidence: low
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A consistent alteration in platelet APP isoforms has been found in Alzheimer disease and Down syndrome. 3 key findings →
Evidence: low
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Stem cells are central to the development and maintenance of many tissues. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Reduced spine densities and age-dependent accumulation of amyloid β and tau pathology are shared features of Down syndrome (DS) and Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The gene encoding the beta-site amyloid precursor protein cleaving enzyme 2 (BACE2) has been determined to be located on the long arm of chromosome 21 at 21q22.3. 5 key findings →
Evidence: low
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Our observations suggest functional tau disturbance in DS brains during development, rather than axonal loss. 1 key finding →
Evidence: low
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Down syndrome (DS), the most common cause of intellectual disability of genetic origin, is characterized by alterations in central nervous system morphology and function that appear from early prenatal stages. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age dependent Alzheimer-type neurodegeneration. 5 key findings →
Evidence: low
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Because of an extra copy of the Aβ precursor protein gene on chromosome 21, Down syndrome (DS) individuals develop high levels of Aβ peptides and Alzheimer disease-like brain amyloidosis early in life. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Trisomy 21 (Down syndrome) is associated with a high incidence of Alzheimer disease and with deficits in cholinergic function in humans. 3 key findings →
Evidence: low
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Down syndrome, caused by the trisomy of chromosome 21, is a complex condition characterized by a number of phenotypic features, including reduced neuron number and synaptic plasticity, early Alzheimer disease-like neurodegeneration, craniofacial dysmorphia, heart development defects, increased incidence of childhood leukemia, and powerful suppression of the incidence of most solid tumors. 3 key findings →
Participants: 1,661 Evidence: low
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Senile myoclonic epilepsy of Genton is a newer epileptic syndrome of the older patients with Down syndrome associated with an Alzheimer-type dementia. 1 key finding →
Evidence: low
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We report on the clinical and cytogenetic assessment of five cases of Down syndrome phenotype with either a partial duplication of chromosome 21 or a normal karyotype, and we quote a case of del (21q) syndrome. 5 key findings →
Evidence: moderate
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Our results provide further insights into the architecture and underlying mechanisms of complex rearrangements on acrocentric chromosomes. 3 key findings →
Evidence: low
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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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Alzheimer's disease (AD) may affect in excess of 90% of individuals with Down syndrome (DS) after age 60, due to duplication of the APP gene in trisomy of chromosome 21, with neuropathology that is comparable to Sporadic AD and Familial AD (FAD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Direct measurements of lysosomal pH uncovered a significant elevation (0.6 units) as a basis for slowed LC3 turnover and the inactivation of cathepsin D and other lysosomal hydrolases known to be unstable or less active when lysosomal pH is persistently elevated. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals with Down syndrome (DS) have an increased risk of early-onset Alzheimer's Disease (AD), largely owing to a triplication of the APP gene, located on chromosome 21. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The management of dementia in Alzheimer's disease has dramatically changed since the development of anti-dementia drugs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The association cortex of Down's syndrome (DS) predictably and prematurely undergoes neurofibrillary degeneration of Alzheimer type. 3 key findings →
Evidence: low
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Progressive electroencephalographic disorganization and decreased voltage amplitude in the late components of the averaged visual evoked potentials were recorded in the last two years of life of a patient with Down disease and Alzheimer degeneration. 3 key findings →
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 →