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Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma proteins affect biological processes and are common drug targets but their role in the development of Alzheimer's disease and related dementias remains unclear. 4 key findings →
Design: cohort study Evidence: moderate
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61/100
Three survey rounds included 49 to 54 participants that agreed on VasCog-2 diagnostic criteria for preclinical, mild, and major dementia levels of vascular cognitive impairment (under the overarching term VCID). 5 key findings →
Participants: 49 Evidence: low
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A distinct set of midlife depressive symptoms was associated with an increased risk of dementia, suggesting that these symptoms might be early markers of underlying neurodegenerative processes. 4 key findings →
Design: cohort Participants: 5,811 Evidence: moderate
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An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course. 4 key findings →
Participants: 39 Evidence: moderate
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Type 2 diabetes is associated with increased risks of cognitive dysfunction and brain abnormalities. 4 key findings →
Participants: 10,663 Evidence: low
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Neuro-inflammation was not reduced between the neflamapimod and placebo groups, and no change was observed in [18F]-DPA-714 PET. 5 key findings →
Design: randomized controlled trial Participants: 17 Evidence: high
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14 IPD-Work studies were assessed and six studies were excluded due to missing outcome data and unavailable data for pooling, resulting in the inclusion of eight studies with 124 909 participants. 5 key findings →
Participants: 909 Evidence: low
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We included 394,255 individuals including 184 incident cases of CD and 459 of UC after median follow-up of 13.6 years (4,889,910 person-years). 5 key findings →
Participants: 394,255 Evidence: moderate
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57/100
Current dementia risk scores have had limited success in consistently identifying at-risk individuals across different ages and geographical locations. 4 key findings →
Participants: 176 Evidence: moderate
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57/100
Ninety-one reviews provided evidence on the impact of telemedicine in dementia care. 5 key findings →
Design: meta-analysis Evidence: high
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). Moreover, 12 proteins related to endothelial function and inflammation were associated with neuroimaging features of SVD. 4 key findings →
Design: cross-sectional Participants: 35 Evidence: moderate
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56/100
The psychostimulant properties of caffeine appear to reduce cognitive decline in women without dementia, especially at higher ages. 2 key findings →
Evidence: moderate
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The increasing number of people with dementia globally illustrates the urgent need to reduce dementia's scale and impact. 1 key finding →
Evidence: low
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Cerebral small vessel disease (SVD) is recognized as a major vascular contributor to cognitive decline, ultimately leading to dementia and stroke. 1 key finding →
Design: longitudinal study Evidence: moderate
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'Covert' cerebral small vessel disease (ccSVD) is common on neuroimaging in persons without overt neurological manifestations, and increases the risk of future stroke, cognitive impairment, dependency, and death. 3 key findings →
Evidence: high
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53/100
Cohort 1 included 446 individuals (mean age (SD) 65.2 years (8.9); 203 women), Cohort 2 included 164 individuals (mean age (SD) 49.9 years (12.6); 88 women). 5 key findings →
Design: longitudinal study Participants: 446 Evidence: moderate
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Comparing clinical stages, CSF PDGFRβ levels were increased at the MCI stage (Cohen's d = 0.55 [CI 95% 0.066, 1.0], P = 0.025) compared with NC. 3 key findings →
Participants: 23 Evidence: low
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51/100
The final study sample comprised 8,797 participants (53.5% women, mean age at HUNT4 77.8 [SD 6.2]). 5 key findings →
Participants: 8,797 Evidence: low
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
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Current AT(N) stratification for Alzheimer's disease (AD) accounts for complex combinations of amyloid (A), tau proteinopathy (T) and neurodegeneration (N) signatures. 4 key findings →
Evidence: moderate
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MEG 16-38Hz spectral power, particularly over parieto-occipital magnetometers, was significantly reduced in the AD progression group. 5 key findings →
Participants: 117 Evidence: low
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By 2040 more people in Scotland are projected to die with palliative care needs, and the complexity of need will increase markedly. 3 key findings →
Participants: 34 Evidence: low
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Our study shows that ICERS of PFA combined with MI and MI alone amounted to €21,443 and €21,543 respectively per improved Z score point compared to the placebo and are below the WTP of €50,000 while the ICER of PFA alone amounted to €111,720 per improved Z score point. 3 key findings →
Participants: 1,525 Evidence: high
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The SorLA protein, encoded by the Sortilin-related receptor 1 ( SORL1 ) gene, is a major player in Alzheimer’s disease (AD) pathophysiology. 4 key findings →
Participants: 30 Evidence: low
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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 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 →