28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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Este trabalho é uma revisão de literatura que explora a relação entre mecanismos epigenéticos e a Doença de Alzheimer (DA), uma doença neurodegenerativa caracterizada por perda de memória e dificuldades cognitivas. 5 key findings →
Evidence: low
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Apolipoprotein E-4 (APOE-4), serotonin transporter gene (SLC6A4), and single nucleotide polymorphisms (SNPs) of glucocerebrosidase (GBA) are some of the main altered genes in AD, PDD and DLB. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a neurological illness that impacts mental and emotional functions functions, has become a global concern due to its increasing prevalence. 2 key findings →
Evidence: low
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Bệnh Alzheimer (AD) có căn nguyên không rõ ràng. 5 key findings →
Evidence: low
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Full or partial trisomy of human chromosome 21 results in dysregulation of gene expression, leading to the manifestation of specific phenotypes described in individuals with Down syndrome (DS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A Doença de Alzheimer (DA) constitui um dos maiores desafios de saúde pública devido ao seu impacto crescente na população idosa, especialmente em razão do aumento da expectativa de vida. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Benzene-1,3-disulfonic acid exhibited strong binding to the Arg136-containing pocket with a top docking score of -5.93 kcal/mol and an estimated inhibition constant (Ki) of 44.6 µmol. 5 key findings →
Evidence: low
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One of the biggest health issues of the twenty-first century is Alzheimer's disease (AD), which is the most prevalent cause of dementia. 1 key finding →
Evidence: low
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A Doença de Alzheimer (DA) é uma enfermidade neurodegenerativa progressiva e a principal causa de demência em idosos, representando cerca de 60 a 70% dos casos. 5 key findings →
Evidence: low
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A Doença de Alzheimer (DA) é uma patologia neurodegenerativa de caráter progressivo, marcada pela deterioração gradual das funções cognitivas e motoras do indivíduo, com o consequente comprometimento da memória, da linguagem e do comportamento. 5 key findings →
Evidence: low
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La presente revisión bibliográfica analiza el papel de la genética clínica en el diagnóstico y pronóstico de la enfermedad de Alzheimer, con un énfasis especial en el contexto ecuatoriano. 5 key findings →
Evidence: low
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Alzheimer disease involves interacting mechanisms that include amyloid-beta accumulation, abnormal tau phosphorylation and aggregation, cholinergic dysfunction, synaptic degeneration, neuronal loss, neuroinflammation, vascular pathology, and genetic susceptibility. 5 key findings →
Design: narrative review Evidence: low
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Alzheimer disease is characterized by gradual and progressive neurodegeneration caused by neuronal cell death. 5 key findings →
Evidence: low
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Down syndrome (DS), caused by trisomy of chromosome 21, exhibits significant phenotypic variability, including intellectual disability, early-onset Alzheimer disease (AD), congenital heart defects (CHDs), haematological malignancies, and immune dysregulation. 5 key findings →
Evidence: low
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Cognitive and behavioural impairment frequently accompanies motor decline in amyotrophic lateral sclerosis (ALS), with 15% of cases meeting the diagnostic criteria for frontotemporal dementia (FTD). 2 key findings →
Evidence: low
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Structural variants (SVs) are a major source of genetic variation yet remain underexplored in healthy aging and neurodegenerative diseases. 1 key finding →
Evidence: low
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Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus. 3 key findings →
Participants: 493 Evidence: low
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Genetic variation at the TMEM106B locus has been associated with Alzheimers disease (AD) and related neurodegenerative phenotypes, yet its haplotypic architecture remains incompletely resolved. 2 key findings →
Participants: 493 Evidence: low
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Alzheimers disease (AD) is defined by progressive neurodegeneration, yet a substantial fraction of its genetic risk maps to non-neuronal processes. 1 key finding →
Evidence: low
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Examples include subpopulations of CD4+ T cells associated with inflammatory bowel disease, characterized by enrichment for a multi-cytokine phenotype and overlap with the naive NF-kB-activated, central memory, and effector memory CD4+ T subtypes, and subpopulations of microglia associated with Alzheimers disease, characterized by depletion of homeostatic programs and localization to the midtemporal gyrus, dorsolateral prefrontal cortex, and medial entorhinal cortex. 3 key findings →
Evidence: low
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Polygenic and proteomic risk scores are both proposed for pre-symptomatic stratification, yet the extent to which they provide overlapping or complementary information has not been measured across neurodegenerative disease. 3 key findings →
Evidence: moderate
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ImportancePatients are increasingly learning Alzheimers disease (AD) genetic and biomarker results through electronic health portals. 5 key findings →
Participants: 216 Evidence: high
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BackgroundPhenotypic age acceleration (PhenoAgeAccel), derived from PhenoAge, and MetaboHealth are composite exposures of biological ageing and metabolic health associated with dementia-related outcomes. 4 key findings →
Design: longitudinal study Participants: 272 Evidence: moderate
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Multi-trait QTL (xQTL) colocalization has shown great promises in identifying causal variants with shared genetic etiology across multiple molecular modalities, contexts, and complex diseases. 2 key findings →
Participants: 595 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 →