27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
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
Amyloid pathology in aDS individuals is linked to frontal‐predominant atrophy without clear hypometabolism. 5 key findings →
Participants: 29 Evidence: low
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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
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Down syndrome individuals develop abnormalities of most organs, including all the pathological and neurochemical features of Alzheimer's disease, by the early age of 30 yr. Here, we report the isolation and characterization of BACE2, a gene mapping on human chromosome 21q22.3, which is highly similar to a transmembrane aspartyl protease, BACE (for beta-site APP-cleaving enzyme), which is able to catalyze the beta-secretase cleavage of Alzheimer's amyloid precursor protein (APP). 5 key findings →
Evidence: low
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Sixty-eight human fibroblast cell strains were assayed for radioresistant DNA synthesis (RDS), which is defined here as the absence of a steep component of inhibition of DNA synthesis in a dose-response curve when rate of DNA synthesis is plotted against radiation doses from 0 to 20 Gy or more. 2 key findings →
Evidence: low
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Oxidative stress is a phenomenon associated with imbalance between production of free radicals and reactive metabolites (e.g. superoxide and hydrogen peroxide) and the antioxidant defences. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
An important lesion in Alzheimer's disease (AD) patient brains is the neurofibrillary tangle (NFT). 5 key findings →
Evidence: low
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Using immunohistochemical techniques we studied the light microscopic localization of ADAMs (A Disintegrin And Metalloprotease) 10 and 15 in different neocortical areas of the human brain during normal aging, and also in patients with Alzheimer disease (AD) and Down syndrome (DS). 3 key findings →
Evidence: low
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This review discusses the laboratory and clinical research supporting the rationale for the efficacy of donepezil (Aricept USA) in enhancing cognition in autism, Alzheimer disease, Down syndrome, traumatic brain injury, Attention Deficit Hyperactivity Disorder (ADHD), and schizophrenia. 4 key findings →
Evidence: low
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More years of education have been found to be associated with a lower rate of Alzheimer disease (AD) in individuals without intellectual disability. 5 key findings →
Evidence: low
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The total number of neurons and glial cells in the mediodorsal thalamic (MDT) nucleus of four aged females with Down syndrome (DS; mean age 69years) was estimated and compared to six age- and sex-matched controls. 3 key findings →
Evidence: low
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Alzheimer disease (AD) and Down syndrome (DS) brains contain deposits of amyloid-beta peptide that are located extracellularly in the neuropil and in blood vessels walls. 2 key findings →
Evidence: low
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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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Long-term treatment with Peptide 6 enhances the pool of newborn neurons in the dentate gyrus, prevents neuronal loss in CA1 and parietal cortex, preserves the dendritic and synaptic architecture in the hippocampus, and improves performance on a hippocampus-dependent memory task in TBI mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
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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
Full summary, score breakdown and related studies → Original source Full text may need a subscription
9 of the 527 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 9. The same 9 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →