Experimental work regarding corrective actions on chromosomes and genes, and control of gene products is yielding promising results. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Experimental work regarding corrective actions on chromosomes and genes, and control of gene products is yielding promising results. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down Syndrome (DS) is the most common of the chromosomal disorders and manifests abnormalities in several organ systems. 5 key findings →
Evidence: low
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Down syndrome (DS) is the most common genetic cause of cognitive deficits. 5 key findings →
Evidence: low
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S100 beta protein, a member of a Ca(2+)-binding protein family present primarily in the nervous system, affects the survival and differentiation of both neurons and glia cells. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In addition to clinical and neuropathological similarities between Alzheimer's disease and Down syndrome there are genetic and biochemical data which suggest common disease mechanism. 3 key findings →
Participants: 19 Evidence: low
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The average lifespan of individuals with Down syndrome has approximately doubled over the past three decades to 55-60 years. 5 key findings →
Evidence: low
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An increased risk of Alzheimer disease (AD) has been reported in young mothers of Down syndrome (DS) probands. 3 key findings →
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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On the basis of what is known about the neural circuitry essential or normally involved in eyeblink classical conditioning (EBCC), the pattern of neurodegeneration in Huntington's disease (HD) would not appear to interfere with this type of learning. 3 key findings →
Evidence: low
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Immunohistochemical staining with polyclonal antibodies to synthetic amyloid (residues 1-28 of A4) was performed on normal and Down syndrome brains from fetuses to adults. 1 key finding →
Evidence: low
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The present findings demonstrate several fundamental parallels between lens and neuron vesicle trafficking cell biology and development, and suggest that more extensive AbetaPP related vesicle trafficking disease mechanisms may be shared by lens and brain. 4 key findings →
Evidence: low
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A German family with 21 members affected by Alzheimer disease (AD) was studied clinically and genetically. 5 key findings →
Evidence: low
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Monoclonal antibodies (mAbs) D3G6 and C8A5, specific for amino acid residues 160-168 of S182 protein, immunolabeled neurons, ependymal and choroid plexus cells, and myocytes in brain sections from normal subjects and people with Alzheimer disease or Down syndrome and in rats and mice. 3 key findings →
Evidence: low
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Cognitive processes and their decline with aging were studied in individuals with Down Syndrome (DS) and individuals of comparable mental handicap without Down Syndrome (NonDS). 1 key finding →
Evidence: low
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Nascent polypeptide-associated complex (NAC) protein, a heterodimeric complex of alpha- and beta-subunits, prevents mistargeting of nascent polypeptide chains to the endoplasmic reticulum membranes. alpha-NAC has sequence similarities with transcription-regulating proteins and has been reported to function as a transcriptional coactivator potentiating c-Jun-mediated transcription. 4 key findings →
Evidence: low
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Notch signaling is a master controller of the neural stem cell and neural development maintaining a significant role in the normal brain function. 1 key finding →
Evidence: low
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This review discusses the research published in the last five years on the behavioral, genetic, medical, and neuroscience aspects of Down syndrome. 2 key findings →
Evidence: low
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Nardilysin is a metalloprotease that cleaves peptides, such as dynorphin-A, α-neoendorphin, and glucagon, at the N-terminus of arginine and lysine residues in dibasic moieties. 5 key findings →
Evidence: low
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Down's syndrome (DS) is characterized by several pathological aspects leading to an increased susceptibility to cardiovascular diseases, infections, leukemia, endocrine alterations. 1 key finding →
Evidence: low
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In addition to the full-length beta-amyloid peptides (Aβ 1-40/42), several Aβ variants, truncated at their N- or C-termini and bearing different post-translational modifications, have been detected in the brain of Alzheimer´s disease (AD) patients. 2 key findings →
Evidence: low
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Tau protein promotes microtubule assembly. 1 key finding →
Evidence: low
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It is a well established fact that Down Syndrome (DS) individuals have a tendency to develop Alzheimer's disease (AD) (Lott, I.T., Head, E., 2005. 4 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
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is one of the most common genetic diseases. 4 key findings →
Evidence: low
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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 →