27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
As the term limbic-predominant age-related transactive response DNA-binding protein 43 (TDP-43) encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published. 1 key finding →
Evidence: low
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Alzheimer's disease currently has no cure and is usually detected too late for interventions to be effective. 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
Mutations in the human prion protein gene (PRNP) are responsible for hereditary diseases called transmissible spongiform encephalopathies (TSE) and a polymorphic site at codon 129 determines sensitivity to infectious forms of these maladies. 5 key findings →
Evidence: low
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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
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This individual had childhood-onset progressive motor impairment. 5 key findings →
Evidence: low
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Poly(ADP-ribosyl)ation (PARylation), a crucial post-translational modification, is catalyzed by ADP-ribosyltransferases (ARTs) and has significant implications in various cellular processes, including DNA damage response, cell signaling, and immune processes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of note, using large-scale transcriptome and chromatin profiling, we show that T cell shape microglia-specific metabolic plasticity in both genetic and epigenetic resolution. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
When rs140926439 was absent, 0.10% of APOEε2/3 carriers had AD, while 0.43% of APOEε4 carriers or homozygotes had AD. 5 key findings →
Evidence: moderate
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Eight proteins were differently expressed in carriers with larger WMH volumes (Figure 1). 5 key findings →
Evidence: low
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Our findings support apathy and APOE ε4 as robust predictors of conversion to MCI and ADD, and demonstrate novel associations between antidepressant use and conversion. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CWPs consist predominantly of two novel arrangements of type I Aβ filaments, and we have designated them as type Ic and type Id Aβ filaments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Here we present our research design and preliminary results in ADAD mutation carriers and controls. 5 key findings →
Evidence: low
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We identified an interaction between TDP-43 and APOE through immunoprecipitation followed by proteomics in mice, verified in human brain by co- immunoprecipitation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It is associated with intracerebral hemorrhage (ICH), cognitive decline, and gait disturbance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genetic linkage studies suggest that Alzheimer's disease (AD) is genetically heterogeneous and that in several early onset families the disease locus is close to the amyloid precursor protein (APP) gene on chromosome 21. 2 key findings →
Design: clinical trial Evidence: low
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Recent reports suggest that cultivated nonneuronal cells from individuals with Alzheimer disease (AD) and other specific hereditary neurodegenerative disorders show hypersensitivity to DNA-damaging agents such as x-rays and radiomimetic chemicals. 3 key findings →
Evidence: low
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Recent evidences indicate that polymorphisms within the promoter region of the vascular endothelial growth factor (VEGF) gene may elevate the risk for Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Endolysosomal dysfunction has been increasingly implicated in the pathogenesis of neurodegenerative diseases. 4 key findings →
Evidence: low
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We evaluated known AD-associated loci (Bellenguez et al. 2022) and 27 loci reached nominal significance (p < 0.05) in at least one cognitive domain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Presenilin 1 (PSEN1) mutations are the leading cause of early-onset Alzheimer disease (EOAD). 3 key findings →
Evidence: low
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Down syndrome, as a phenotypic result of trisomy 21, is a complex condition with a set of over 30 phenotypic features, which manifest themselves with varying frequencies among affected individuals. 3 key findings →
Evidence: low
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ADAM10 plays a fundamental role in brain function, and sufficient studies support its involvement in AD pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The predALZ framework achieved 94% accuracy on an independent test set and approximately 96% accuracy in cross-validation for Alzheimer-related driver gene prediction. 5 key findings →
Evidence: low
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This diploma thesis presents the work carried out during 6 months within the Laboratory directed by Professor Millet, written under the supervision and with the support of Dr. Benjamin Tournier and Silvia Braconi Quintaje. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,521 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 27,380 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 →