30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
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
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
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
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
Full summary, score breakdown and related studies → Original source Free full text
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
BACE2 is homologous to BACE1, a beta-secretase that is involved in the amyloidogenic pathway of amyloid precursor protein (APP), and maps to the Down syndrome critical region of chromosome 21. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The human ETS2 gene, a member of the ETS gene family, with sequence homology with the retroviral ets sequence of the avian erythroblastosis retrovirus E26 is located on chromosome 21. 5 key findings →
Evidence: low
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Isoprostanes are a recently discovered group of prostaglandin isomers. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Platelets are the main source of 5-hydroxytryptamine (5-HT) and amyloid precursor protein (APP) found in plasma. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Reduced telomere length has recently been reported in T lymphocytes of individuals with trisomy 21 Down syndrome (DS) and dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is an aneuploidy syndrome that is caused by trisomy for human chromosome 21 resulting in a characteristic cognitive and behavioral phenotype, which includes executive functioning and adaptive behavior difficulties possibly due to prefrontal cortex (PFC) deficits. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with Down syndrome develop neuropathologic and in some cases clinical evidence of Alzheimer disease after age 40. 5 key findings →
Evidence: low
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Human trisomy 21 is the most frequent live-born human aneuploidy and causes a constellation of disease phenotypes classified as Down syndrome, which include heart defects, myeloproliferative disorder, cognitive disabilities and Alzheimer-type neurodegeneration. 2 key findings →
Evidence: low
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Experimental work regarding corrective actions on chromosomes and genes, and control of gene products is yielding promising results. 1 key finding →
Evidence: low
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The anterior thalamic nuclei are important for cognition, and memory in particular. 3 key findings →
Evidence: low
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During alteplase administration, the patient experienced clinical deterioration. 5 key findings →
Evidence: low
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The precise regulation of DSCR gene expression is crucial to maintain the brain homeostasis, especially in those areas with high levels of gene expression associated with a remarkable process of learning and cognition. 3 key findings →
Evidence: low
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Recently, an increasing number of genes have been associated with global developmental delay (GDD) and intellectual disability (ID). 5 key findings →
Evidence: low
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How do clinicians distinguish early-stage dementia from the expected cognitive variability seen in ageing adults with Down syndrome? 2 key findings →
Participants: 72 Evidence: low
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Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability. 1 key finding →
Design: narrative review Evidence: low
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For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The 5' untranslated region (UTR) of the APP gene, encompassing 147 base pairs between the transcriptional (+1) and the translational start site, was examined for its role in APP expression. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Paired helical filaments (PHF), which constitute neurofibrillary tangles (NFT) and neuritic plaque (NP) neurites, serve as a useful marker for Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Gene dysregulation in trisomy 21 can cause disorders of genes that are members of the heat-shock proteins (HSPs) family and contribute to the early onset of Alzheimer's disease (AD) in Down syndrome (DS). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events