28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
WMH were associated with increased risk of cognitive dysfunction and could become a neuroimaging indicator of dementia. 3 key findings →
Design: meta-analysis Participants: 19,040 Evidence: high
Full summary, score breakdown and related studies → Original source
CSF Aβ42, t-tau, p-tau, tau/Aβ42; peripheral blood t-tau, Aβ42/Aβ40, NFL; whole, left and right HV, EC volume, MTA, 18 F-FDG PET, 11 C-PIB PET; APOE ε4 may be promising prospective biomarkers for AD progression. 3 key findings →
Design: meta-analysis Participants: 70 Evidence: high
Full summary, score breakdown and related studies → Original source
Patients with MCI with APOEε4, abnormal CSF τ level, hippocampal and medial temporal lobe atrophy, entorhinal atrophy, depression, diabetes, hypertension, older age, female gender, lower MMSE score and higher ADAS-cog score, had a high risk for the progression to AD. 1 key finding →
Design: meta-analysis Participants: 14,821 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Significantly altered levels of inflammatory markers were verified in comparison between AD, MCI and control, supporting the notion that AD and MCI are accompanied by inflammatory responses in both the periphery and CSF. 5 key findings →
Design: systematic review Participants: 170 Evidence: high
Full summary, score breakdown and related studies → Original source
Low SES substantially increased the risk of dementia and cognitive dysfunction, suggesting that public health strategies could reduce the dementia burden by reducing social inequalities. 4 key findings →
Design: meta-analysis Participants: 1,485,702 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In our study, in addition to PD, NFL was suggested to be a global diagnostic biomarker for neurodegenerative diseases. 4 key findings →
Design: meta-analysis Participants: 36 Evidence: high
Full summary, score breakdown and related studies → Original source
Dementia is a severe neurodegenerative disorder and it can be categorized into several subtypes by different pathogenic causes. 3 key findings →
Participants: 10,000 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Early-life factors, including education level, leg length, history of childhood head trauma, family-related factors and learning ability, were associated with the risk of dementia and cognitive impairment in later life. 3 key findings →
Design: systematic review Participants: 46,727 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Diabetes, even prediabetes and changes of diabetes-related biochemical indicators, predicted increased incidence of cognitive impairment and dementia. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Controversies persist regarding the association between blood pressure (BP) and the risks of cognitive impairment and dementia due to inconsistent definitions of BP exposure and varying population characteristics. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Sleep management might serve as a promising target for dementia prevention. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The development of blood-based biomarkers of Alzheimer's disease (AD) pathology as tools for screening the general population is essential, but persists controversies. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
This review highlights that air pollutions, especially PM 2.5 and NO 2 play important role in the risk for age-related cognitive impairment and dementia. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Plasma phosphorylated-tau181 (p-tau181) showed the potential for Alzheimer's diagnosis and prognosis, but its role in detecting cerebral pathologies is unclear. 3 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
Full summary, score breakdown and related studies → Original source
Observational studies support the use of NSAIDs for prevention of AD, but RCT do not. 4 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Controversies persist about the associations of body mass index (BMI) with risk of cognitive impairment and dementia. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Dietary patterns and some dietary components have been linked with dementia. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Sunlight exposure had a J-shaped association with dementia risk. 2 key findings →
Design: prospective cohort Evidence: moderate
Full summary, score breakdown and related studies → Original source
Effective interventions in diet, medications, biochemical exposures, psychological condition, pre-existing disease and lifestyle may decrease new incidence of AD. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
NPS were observed to be highly prevalent in AD patients. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
TREM2 (triggering receptor expressed on myeloid cells 2) gene variants were reported to increase the risk of Alzheimer's disease (AD) and even other neurodegenerative diseases (frontotemporal dementia (FTD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS)), but so far, no definite conclusion has been drawn. 4 key findings →
Design: systematic review Participants: 39 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We have reported, for the first time, the dose-response relationship between LTPA and dementia, further supporting the international PA guideline from the standpoint of dementia prevention. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
To assess plasma phosphorylated tau181 (p-tau181) as a progression biomarker in Alzheimer's disease (AD), we examined longitudinal plasma p-tau181 of 1184 participants (403 cognitively normal (CN), 560 patients with mild cognitive impairment (MCI), and 221 with AD dementia) from Alzheimer's Disease Neuroimaging Initiative (ADNI). 4 key findings →
Design: longitudinal study Participants: 1,184 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The relationship between mild behavioral impairment (MBI) and Alzheimer's disease (AD) is intricate and still not well investigated. 4 key findings →
Design: longitudinal study Participants: 1,129 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma NfL level is a valuable noninvasive biomarker that supplements magnetic resonance imaging scans and possibly reflects the severity of CSVD burden. 3 key findings →
Design: cross-sectional Participants: 496 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
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.
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 28,580 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →