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
Research
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Introducción: La neuroinflamación ha adquirido creciente relevancia en la fisiopatología de la enfermedad de Alzheimer por su interacción con la acumulación de β-amiloide, la patología tau, la disfunción sináptica y la neurodegeneración. Microglía, astrocitos y múltiples vías de señalización inmunitaria constituyen potenciales dianas terapéuticas. 5 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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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
Full summary, score breakdown and related studies → Original source Free full text
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
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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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ResumenLa llegada de los anticuerpos monoclonales lecanemab y donanemab marca un cambio de paradigma en el tratamiento de la enfermedad de Alzheimer, transitando del nihilismo terapéutico a la era de las terapias modificadoras de la enfermedad. 1 key finding →
Evidence: low
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Alzheimer disease (AD) pathology affects the transentorhinal/entorhinal region early but whether entorhinal cortex (EC) astrocytes are causal drivers or therapeutic targets remains unresolved. 5 key findings →
Design: narrative review 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
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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
Full summary, score breakdown and related studies → Original source Free full text
Resumen Introducción La vía amiloidogénica de procesamiento de la proteína precursora del amiloide es bien conocida a nivel de patogenia y terapéutica en la enfermedad de Alzheimer (EA), mientras que la vía no-amiloidogénica ha sido menos estudiada. 5 key findings →
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
Full summary, score breakdown and related studies → Original source Free full text
27/100
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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El desarrollo de biomarcadores plasmáticos ha revolucionado el diagnóstico biológico de la enfermedad de Alzheimer (EA), al permitir una detección más temprana y menos invasiva de los procesos neuropatológicos subyacentes. 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
Full summary, score breakdown and related studies → Original source Free full text
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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Yeni bilimsel araştırma, Alzheimer hastalığının %90’ından fazlasının APOE geniyle bağlantılı olabileceğini ortaya koydu. 2 key findings →
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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La enfermedad de Alzheimer (EA) es la demencia neurodgenerativa más prevalente a nivel mundial, en los últimos años se ha resaltado su relación con los trastornos del sueño y la desregulación de la melatonina. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 29,380 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →