BAN2401-G000-201 did not meet the 12-month primary endpoint. 5 key findings →
Design: clinical trial Participants: 18 Evidence: high
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.
Greater consumption of caffeinated coffee and tea was associated with lower risk of dementia and modestly better cognitive function, with the most pronounced association at moderate intake levels. 5 key findings →
Design: cohort Participants: 131,821 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Evidence suggests that lifelong cumulative exposure to pesticides may generate lasting toxic effects on the central nervous system and contribute to the development of Alzheimer's disease (AD). 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
71/100
Polysomnography (PSG) studies of sleep changes in Alzheimer's disease (AD) have reported but not fully established the relationship between sleep disturbances and AD. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
70/100
In this prospective cohort study, higher consumption of UPF was associated with higher risk of dementia, whereas substituting unprocessed or minimally processed foods for UPF was associated with lower risk of dementia. 5 key findings →
Design: cohort Participants: 72,083 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Overall, our analysis revealed a robustly defined age-related co-methylation module that is present in multiple human tissues, including blood and brain. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Intake of coffee alone or in combination with tea was associated with lower risk of poststroke dementia. 3 key findings →
Design: cohort study Participants: 365,682 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (APOE) ε4 is the single most important genetic risk factor for cognitive impairment and Alzheimer disease (AD), while lifestyle factors such as smoking, drinking, diet, and physical activity also have impact on cognition. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The advent of proteomics offers an unprecedented opportunity to predict dementia onset. 1 key finding →
Participants: 52,645 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results demonstrate an important role of clusterin in the pathogenesis of AD and suggest that alterations in amyloid chaperone proteins may be a biologically relevant peripheral signature of AD. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a devastating neurodegenerative disorder with no cure, and available treatments are only able to postpone the progression of the disease. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Social determinants of health (SDHs) are the primary drivers of preventable health inequities, and the associations between SDHs and health outcomes among individuals with type 2 diabetes remain unclear. 4 key findings →
Design: cohort study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Delirium is a frequent complication in older ICU patients and often persists beyond their ICU stay. 3 key findings →
Design: cohort study Participants: 45 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The cytoplasmic mislocalization and aggregation of TAR DNA-binding protein-43 (TDP-43) is a common histopathological hallmark of the amyotrophic lateral sclerosis and frontotemporal dementia disease spectrum (ALS/FTD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
59/100
Assessment of the cingulum fibers using diffusion tensor imaging may aid early diagnosis of Alzheimer disease. 4 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
59/100
From 2011 to 2013, 1,744 participants completed high-resolution vessel wall MRI from the population-based Atherosclerosis Risk in Communities Study by a sampling strategy that allowed weighting back to the cohort. 4 key findings →
Participants: 291 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Previous hypothesis-driven research has identified many risk factors linked to dementia. 4 key findings →
Participants: 344,324 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The AD set included 23,092 cases and 30,920 controls, the ALS set included 7391 cases and 12,442 controls, and the PD set included 8498 patients and 9161 controls. 3 key findings →
Design: meta-analysis Participants: 23,092 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Plasma-based biomarkers would be potential biomarkers for early diagnosis of Alzheimer's disease (AD) because they are more available and cost-effective than cerebrospinal fluid (CSF) or neuroimaging. 4 key findings →
Design: cross-sectional Participants: 185 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Parkinson disease is a common neurodegenerative disorder characterized by the loss of dopaminergic neurons and the presence of intracytoplasmic-ubiquitinated inclusions (Lewy bodies). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
It has been well established that the TMEM106B gene rs1990622 variant was a frontotemporal dementia (FTD) risk factor. 4 key findings →
Participants: 314,278 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Abnormal plasma Aβ42/40 ratio identified older adult groups with lower memory scores, higher dementia risks, and higher ADRD biomarker levels, with potential implications for population screening. 2 key findings →
Participants: 847 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is one of the most common diseases among the older adults. 5 key findings →
Participants: 45 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Developing a single-domain assay to identify individuals at high risk of future events is a priority for multi-disease and mortality prevention. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E E4 allele of the APOE gene is the strongest genetic factor for late-onset Alzheimer disease (LOAD). 3 key findings →
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 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 →