39/100
We highlight a general overview and methodology of TNS. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The lack of significant results for moderation effects of the targeted epigenetic markers in our pilot study were likely due to the small sample size. 5 key findings →
Participants: 812 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) diagnosis is confirmed using a medley of modalities, such as the detection of amyloid-β (Aβ) neuritic plaques and neurofibrillary tangles with positron electron tomography (PET) or the appraisal of irregularities in cognitive function with examinations. 3 key findings →
Participants: 53 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
39/100
We have successfully generated specific high affinity monoclonal antibodies against p -Tau217, p -Tau205, and N-terminus GFAP and have confirmed that these antibodies have the necessary specificity and sensitivity for the Simoa platform. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia disproportionately affects Hispanic/Latino caregivers, and while some interventions exist, their consideration of intersectional factors remains unclear. 1 key finding →
Participants: 41 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology. 3 key findings →
Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology. 3 key findings →
Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
39/100
Tauopathies are neurodegenerative disorders characterized by the abnormal accumulation and aggregation of hyperphosphorylated tau protein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
39/100
Several concepts, which in the aggregate get might be used to account for "resilience" against age- and disease-related changes, have been the subject of much research.
Full summary, score breakdown and related studies → Original source
Stem cells are central to the development and maintenance of many tissues. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Social determinants of health, such as neighborhood disadvantage, have been linked to an increased risk of clinical dementia syndrome; however, their association with neuropathologically confirmed Alzheimer's disease (AD) remains unknown. 5 key findings →
Participants: 434 Evidence: low
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Reducing Alzheimer disparities and generating the evidence needed to promote brain health for everyone requires diverse research representation, including areas near an ADRC. 3 key findings →
Participants: 428 Evidence: low
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Biomarkers serve as a quantitative measure of brain injury and may predict cognitive outcome after cardiac arrest. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The majority of the participants met criteria for obesity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CVD risk has been associated with white matter lesions known as white matter hyperintensities (WMH) because they produce increased signal on fluid‐attenuated inversion recovery (FLAIR) MRI scans. 5 key findings →
Participants: 804 Evidence: moderate
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In UKB, PRS cancer was nominally associated with improved fluid intelligence ( β : 0.12, 95% CI: 0.01-0.22). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tau protein misfolding and deposition in the brain is a common factor across many neurodegenerative diseases, grouped under the term tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
36/100
In the last decade, a number of important research advances in different fields have allowed Down syndrome (DS) research to flourish, creating a time of both unparalleled opportunity and considerable challenge. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-β (Aβ) aggregated forms are highly associated with the onset of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Our findings suggest differences in local cortical organization by neighborhood disadvantage, which also mediated the relationship between ADI and cognitive performance, providing a possible network‐based mechanism, explaining risk for cognitive decline and dementia associated with disadvantaged neighborhoods. 3 key findings →
Participants: 526 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest differences in local cortical organization by neighborhood disadvantage, which also mediated the relationship between ADI and cognitive performance, providing a possible network‐based mechanism, explaining risk for cognitive decline and dementia associated with disadvantaged neighborhoods. 3 key findings →
Participants: 526 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The ABC-DS cohort showed similar Aβ PET burden but had a lower prevalence of ApoE4 carriers, younger age at clinical diagnosis and autopsy, shorter PET-autopsy interval, smaller amygdala and hippocampal volumes, more advanced CERAD scores, and no atherosclerosis compared to ADRC cohort (Figure 1). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
35/100
Autosomal dominant Alzheimer disease (ADAD) is caused by pathogenic variants in the APP, PSEN1 and PSEN2 genes, but a substantial fraction of reported variants is of unknown clinical significance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PART and LATE patients exhibit Tau PET uptake similar to that of controls, except in the putamen. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Access is controlled through both technical and procedural methods and overseen by an external advisory committee Results Expo‐AD is currently storing personal identifiers and neuropathology data of 10,875 brain donors acquired from 22 participating brain banks and the National Alzheimer’s Coordinating Center. 1 key finding →
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 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.
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 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 →