27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
(1) GARS-AIRS-GART is an important candidate gene in studies of Down syndrome (DS)-related Alzheimer's disease (AD), due to its chromosomal localization (21q22.1) in the Down syndrome critical region, involvement in de novo purine biosynthesis, and over-expression in DS brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 21, is the most frequent genetic cause of intellectual disability worldwide. 1 key finding →
Design: narrative review Evidence: low
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Studies in Jalisco have identified a mutation in the PSEN1 gene, associated with early-onset Alzheimer's. This variant, common in the Altos de Jalisco region, affects both men and women, causing severe symptoms such as difficulty walking and speaking. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Esse artigo buscou abordar a Doença de Alzheimer de Início Precoce (DAIP) acerca do curso clínico, dos fatores predisponentes e do manejo, por meio de uma revisão de literatura, com ênfase na diferenciação entre DAIP e Doença de Alzheimer de Início Tardio (DAIT), incluindo artigos publicados entre 2015 e 2025, obtidos nas bases de dados “Alzheimer's Association”, “ScienceDirect”, “Cochrane” e “PubMed”, utilizando as palavras-chave “Alzheimer”, “early” e “on-set”, com o conectivo AND. 4 key findings →
Evidence: low
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Sequencing revealed a biallelic SORL1 splice donor variant (c.1211 + 1G > A). 5 key findings →
Evidence: low
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El objetivo de este trabajo es desarrollar un algoritmo de forrajeo de bacterias para el alineamiento múltiple de secuencias genéticas. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We have reported recently the sublocalization of an Alzheimer Disease-associated gene that encodes for cerebrovascular beta-amyloid protein (BAP). 2 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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Alzheimer's disease progresses heterogeneously across diverse cohorts, yet current predictive models fail to capture this complexity while remaining clinically interpretable. 4 key findings →
Design: longitudinal study Participants: 1,669 Evidence: moderate
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Alzheimer’s disease manifests through heterogeneous progression patterns across diverse populations, yet current predictive models fail to capture this complexity while maintaining clinical interpretability. 4 key findings →
Design: longitudinal study Participants: 1,669 Evidence: moderate
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Directed conversion of mature human cells, as from fibroblasts to neurons, is of potential clinical utility for neurological disease modeling as well as cell therapeutics. 2 key findings →
Evidence: low
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Alzheimer disease (AD) is a heterogeneous disease with many genes are associated with AD risk. 4 key findings →
Participants: 360 Evidence: low
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Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →
Participants: 484 Evidence: low
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We estimated associations of educational attainment and Alzheimer disease genetic risk with treatment initiation and incident dementia and compared GLP-1 receptor agonist initiators with initiators of non-sodium-glucose cotransporter 2 inhibitor second-line therapies, with a separate sodium-glucose cotransporter 2 inhibitor compa 4 key findings →
Design: cohort study Participants: 14,364 Evidence: moderate
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Mounting evidence suggests that defects in energy metabolism contribute to the pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →
Design: longitudinal study Participants: 22,825 Evidence: moderate
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Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia. 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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Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood. 1 key finding →
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
Full summary, score breakdown and related studies → Original source Free full text
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
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. 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 →