28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Lysosome dysfunction arises early and propels Alzheimer’s Disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There was a significant interaction between OSA and diagnosis for within- and between-DMN FC (p-values<0.05). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The ABC-DS cohort showed similar Aβ PET burden but had a lower prevalence of ApoE4 carriers, younger age at clinical diagnosis and autopsy, shorter PET-autopsy interval, smaller amygdala and hippocampal volumes, more advanced CERAD scores, and no atherosclerosis compared to ADRC cohort (Figure 1). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyloid pathology in aDS individuals is linked to frontal‐predominant atrophy without clear hypometabolism. 5 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MOLDI-MS identified eighty-five proteins represented by multiple tryptic peptides, twenty-five of which showed significant differences between DS and controls, confirmed by WB and ELISA analysis. 5 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nitric oxide (NO) and carbon monoxide (CO) synthesized from L-arginine by NO synthase and from heme by heme oxygenase, respectively, are the well-known neurotransmitters and are also involved in the regulation of vascular tone. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome is one of the major causes of mental retardation and congenital heart malformations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent findings link altered processing of beta-amyloid precursor protein (beta APP) to disruption of neuronal Ca2+ homeostasis and an excitotoxic mechanism of cell death in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hydrogen sulfide is one of three gases involved in biological functions and synthesized in vivo. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Endocytosis is universally important in cell function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulating evidence points to an important role of intraneuronal A beta as a trigger of the pathological cascade of events leading to neurodegeneration and eventually to Alzheimer's disease (AD) with its typical clinical symptoms, like memory impairment and change in personality. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
An additional copy of the beta-amyloid precursor protein (APP) gene causes early-onset Alzheimer's disease (AD) in trisomy 21 (DS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals with Down syndrome (DS) commonly possess unique neurocognitive and neurobehavioral profiles that emerge within specific developmental periods. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of amyloid beta-protein (Abeta) is a fundamental feature of certain human brain disorders such as Alzheimer's disease (AD) and Down syndrome and also of the skeletal muscle disorder inclusion body myositis (IBM). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human cellular models of Alzheimer's disease (AD) pathogenesis would enable the investigation of candidate pathogenic mechanisms in AD and the testing and developing of new therapeutic strategies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglial cells and astrocytes are closely associated with nearly all compact deposits of the amyloid beta-protein found in the senile plaques characteristic of Alzheimer's disease and trisomy 21. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormalities of zinc homeostasis occur in Alzheimer's disease (AD), a dementia characterized by the aggregation of A beta in the brain, and in Down syndrome, a condition characterized by premature AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) brains display A beta (Abeta) plaques, inflammatory changes and neurofibrillary tangles (NFTs). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Altered neuronal endocytosis is the earliest known pathology in sporadic Alzheimer's disease (AD) and Down syndrome (DS) brain and has been linked to increased Abeta production. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammatory conditions such as traumatic brain injury, aging, Alzheimer's disease, and Down syndrome are often associated with cognitive dysfunction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is characterized by increased mortality rates, both during early and later stages of life, and age-specific mortality risk remains higher in adults with DS compared with the overall population of people with mental retardation and with typically developing populations. 2 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 →