In total, 881 (21.6%) participants had ILF and 272 (6.8%) participants developed dementia. 5 key findings →
Participants: 4,072 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
= 0.007) in AD-signature regions and a numerically higher burden of vascular risk factors. 5 key findings →
Participants: 1,214 Evidence: moderate
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Collectively, these findings suggest that Aβ promotes gut symptoms through alteration of ENS connectivity and butyrate counteracts these impairments with an amelioration of neuroinflammation and memory function in AD model. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
O]water PET were strongest for 1800 msec single-PLD and generally decreased with longer PLDs, except the occipital lobe, where all PLDs showed poor agreement. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In the cohort, 39.2% (67/171) tested positive by α-syn SAA. α-syn SAA positivity was more frequently detected alone than in combination with biomarkers of AD pathology (25.1% vs. 14.0%). α-syn SAA+ status was independently associated with higher odds of fluctuating cognition (OR 2.99, 95%CI 1.46–6.25, p = 0.012), visual hallucinations (OR 2.41, 95%CI 1.24–4.75, p = 0.027), extrapyramidal signs (OR 4.57, 95%CI 2.35–9.11, p < 0.001) and akinetic mutism (OR 3.77, 95%CI 1.22–12.82, p = 0.038). 5 key findings →
Participants: 171 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
After deduplication and screening of 8893 records, we included 109 studies describing a wide array of wearable or portable DHTs that obtained digital biomarkers. 5 key findings →
Participants: 109 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the central Lewy body diseases (LBDs) Parkinson's disease and dementia with Lewy bodies (DLB), by the time parkinsonism or cognitive dysfunction manifests, substantial central neurodegeneration has already occurred. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The prevalence of PIMcogs increased from 16% at baseline to 23% at follow-up. 5 key findings →
Participants: 397 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Disruptions in GABAergic activity and alterations in gamma oscillations are key pathological features of AD associated with amyloid-beta (Aβ) plaques. 3 key findings →
Design: longitudinal study Participants: 127 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
After adjusting for potential confounders, multivariable logistic regression models revealed that the prevalence of dementia was significantly higher in individuals with chronic pain than in those without. 3 key findings →
Design: cross-sectional Participants: 1,096 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this retrospective, confounder-adjusted study, anticoagulation was associated with slower cognitive/functional decline and lower hospitalization/mortality risk in AF and dementia patients. 3 key findings →
Design: cohort study Participants: 291 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
= 0.015). In this autopsy-confirmed cohort, seizure susceptibility was associated with advanced tau pathology and CAA in AD. 4 key findings →
Design: cohort study Evidence: moderate
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At baseline, the mean MNA score was 22.5 ± 2.3. 5 key findings →
Participants: 105 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Of 574 older adults, 187 (33%) were admitted. 5 key findings →
Participants: 574 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is responsible for 70% of dementia cases worldwide, with tau hyperphosphorylation and amyloid-β plaque accumulation representing its core pathological hallmarks. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
IBD is associated with CI and increased dementia risk, with biologics potentially mitigating neuroinflammation-related decline. 4 key findings →
Design: systematic review Evidence: high
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Alzheimer's disease (AD) and cancer are among the most devastating diseases worldwide. 2 key findings →
Evidence: early
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Presence of CHD may influence AD progression in DS. 1 key finding →
Participants: 82 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
48/100
Individuals with Down syndrome (DS) have an increased risk of developing Alzheimer disease (AD), with nearly all individuals exhibiting AD neuropathology, including amyloid beta (Aβ) plaques and neurofibrillary tangles (NFT), by age 40 years. 5 key findings →
Design: cross-sectional Participants: 98 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with autosomal dominant Alzheimer's disease (ADAD) arising from mutations in PSEN1, PSEN2, or APP exhibit variability in clinical presentation. 4 key findings →
Participants: 2,338 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that non-economic social deprivation, especially in terms of access to a grocery store, pharmacy, postal office, and bus stop, might be relevant for maintaining cognitive functioning in old age. 4 key findings →
Design: longitudinal study Participants: 91 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of the 508 eligible MA enrollees, mean age was 82.8 (SD = 7.2) years, 81% were female, and 49% were non-Latino White; 62 participants (12%) were classified as having dementia by the cohort assessment. 5 key findings →
Design: cohort study Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Thirty-three AD subjects, aged 69.3 ± 8.2 years (mean ± standard deviation), 18 females, and 22 HCs aged 70.5 ± 13.3 years, 15 females, were evaluated. 5 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Older age was associated with greater odds of abnormal p-Tau217 (odds ratio [OR] 1.08 per year, 95% CI 1.07–1.09), as was APOE ε4 carrier status (OR 3.32, 95% CI 2.65–4.17). 5 key findings →
Design: cross-sectional Participants: 2,798 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This longitudinal evidence supports a link between the ALPS-I and cognitive degeneration. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 27,380 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 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 →