The Alzheimer's Association hosted the second Latinos & Alzheimer's Symposium in May 2021. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Recent evidence suggests that rare genetic variants within the TREM2 gene are associated with increased risk of Alzheimer's disease. 4 key findings →
Evidence: moderate
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In the within-language condition, combined speech timing and lexico-semantic features yielded maximal classification (area under the receiver operating characteristic curve [AUC]=0.88), outperforming single-feature models (AUC=0.79 for timing features; AUC=0.80 for lexico-semantic features). 5 key findings →
Participants: 211 Evidence: low
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We recruited 1501 participants (304 with FTLD, 512 with AD, and 685 healthy controls) from the Multi-Partner Consortium to Expand Dementia Research in Latin America (ReDLat). 5 key findings →
Participants: 1,501 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
50/100
The Dominantly Inherited Alzheimer Network Observational Study (DIAN Obs) is a longitudinal, global cohort study investigating brain aging and autosomal dominant Alzheimer’s disease (ADAD), a rare monogenic form of Alzheimer’s disease (AD). 5 key findings →
Design: cohort study Evidence: moderate
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The blood-brain barrier (BBB) is a tightly regulated interface in the Central Nervous System (CNS) that regulates the exchange of molecules in and out from the brain thus maintaining the CNS homeostasis. 4 key findings →
Evidence: low
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Clinical trials of anti-amyloid-β (Aβ) monoclonal antibodies in Alzheimer disease (AD) infer target engagement from Aβ positron emission tomography (PET) and/or fluid biomarkers such as cerebrospinal fluid (CSF) Aβ42/40. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Latin America’s diverse genetic landscape provides a unique opportunity to study Alzheimer’s disease (AD) and frontotemporal dementia (FTD). 1 key finding →
Participants: 2,162 Evidence: low
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In the LA cohort only, higher WMHs load was associated with greater GM atrophy across all groups (HCs, AD, bvFTD), with a specific neurodegenerative pattern involving orbitofrontal, cingulate, and temporal areas. 5 key findings →
Participants: 402 Evidence: moderate
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These findings suggest that OCT can detect functional and morphologic changes in the retina of carriers of familial Alzheimer disease who are cognitively unimpaired several years before clinical onset, suggesting that OCT findings and retinal vascular parameters may be biomarkers prior to the onset of cognitive decline. 4 key findings →
Design: cross-sectional Evidence: low
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We extend prior work using BAG from sporadic AD to ADAD, noting consistent results. 5 key findings →
Evidence: moderate
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Researchers have begun to characterize the subtle biological and cognitive processes that precede the clinical onset of Alzheimer disease (AD), and to set the stage for accelerated evaluation of experimental treatments to delay the onset, reduce the risk of, or completely prevent clinical decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several studies have recently shown that basal ganglia (BG) deterioration leads to distinctive impairments in the domains of syntax, action verbs, and action semantics. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
39/100
The sample included 61 participants (55.7% female), aged 18-58, with a median education of 12 years (IQR: 10-14). 5 key findings →
Participants: 61 Evidence: low
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Astrocytes are specialized glial cells that are essential components of the neurovascular unit (NVU) and are involved in neurodevelopment, brain maintenance and repair, and neurodegeneration. 2 key findings →
Evidence: low
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Our work suggests an anti-inflammatory effect of quercetin in the CA1 hippocampal region of aged triple transgenic Alzheimer's disease mice. 2 key findings →
Evidence: low
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The most notable effect sizes were observed in entropy for Beta1 and Beta3 bands in frontal regions for the DTS7 and DTS1 tasks, Beta2 relative power in C4 during DTAN, Theta modulation in the Theta and alpha-1 bands in frontal regions during DTS7, and Alpha2 modulations in the same task. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The most notable effect sizes were observed in entropy for Beta1 and Beta3 bands in frontal regions for the DTS7 and DTS1 tasks, Beta2 relative power in C4 during DTAN, Theta modulation in the Theta and alpha-1 bands in frontal regions during DTS7, and Alpha2 modulations in the same task. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
La enfermedad de Alzheimer (EA) fue descrita por primera vez en una mujer, Augusta D, cuyo caso reveló las características neuropatológicas clásicas de placas amiloides y ovillos neurofibrilares. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
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.
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
- Randomized / 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
- Multicenter 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events