29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer's disease associated with exposure. 5 key findings →
Design: longitudinal study Participants: 998 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our prediction model was internally evaluated based on five-fold cross-validation on discrimination and calibration, and it was further compared with existing prediction scales. 2 key findings →
Design: longitudinal study Participants: 2,416 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This cohort study found that COVID-19 mortality decreased over time during 2020 and that patient demographic characteristics and comorbidities were associated with higher clinical severity. 5 key findings →
Design: cohort study Participants: 174 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Data collected from clinical trials and cohort studies, such as dementia studies, are often high-dimensional, censored, heterogeneous and contain missing information, presenting challenges to traditional statistical analysis. 1 key finding →
Design: cohort study Participants: 1,037 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
An optimized immunoassay was used to analyze CSF Ng in a retrospective cohort of 331 participants with different neurodegenerative diseases, including healthy controls (n = 19), biomarker-proven Alzheimer disease (AD) (n = 100), genetic AD (n = 2), behavioral variant frontotemporal dementia (n = 20), speech variant frontotemporal dementia (n = 21), Lewy body dementia (n = 13), Parkinson disease (n = 31), progressive supranuclear palsy (n = 46), multiple system atrophy (n = 29), as well as a heterogeneous group with non-neurodegenerative cognitive impairment (n = 50). 1 key finding →
Design: retrospective cohort Participants: 19 Evidence: moderate
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These findings suggest that machine learning algorithms could accurately predict incident dementia within 2 years in patients receiving care at memory clinics using only 6 variables. 5 key findings →
Design: prospective cohort Participants: 307 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We developed machine learning prediction models for post-operative delirium that performed better than chance and are comparable with traditional stepwise logistic regression. 1 key finding →
Design: cohort study Participants: 134 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We conducted the largest metabolome investigation of dementia to date, for the first time revealed the metabolite importance ranking, and highlighted the contribution of plasma metabolites for dementia prediction. 5 key findings →
Design: longitudinal study Participants: 274,160 Evidence: moderate
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Previous studies from our group have shown that language changes may be reflected in connected speech production in the earliest stages of typical Alzheimer's disease. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Digital literacy may help reduce cognitive decline among persons aged between 50 and 89 years. 2 key findings →
Design: longitudinal study Participants: 6,442 Evidence: moderate
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Comorbid cardiovascular and metabolic risk factors (CVM) differentially impact brain structure and increase dementia risk, but their specific magnetic resonance imaging signatures (MRI) remain poorly characterized. 1 key finding →
Design: cohort study Participants: 37,096 Evidence: moderate
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Subjective cognitive decline (SCD) is regarded as the first clinical manifestation in the Alzheimer's disease (AD) continuum. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Graph theoretical analysis of the speech/language network showed that regions with shorter functional paths to the epicentre exhibited greater longitudinal atrophy. 4 key findings →
Design: longitudinal study Participants: 30 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Multiple system tauopathy with presenile dementia (MSTD) is an inherited disease caused by a (g) to (a) transition at position +3 in intron 10 of Tau. 1 key finding →
Design: longitudinal study Participants: 21 Evidence: moderate
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The study consists of 25,186 patients (mean age = 63.0, interquartile range [IQR] of age = 15.1 years, male = 50%). 3 key findings →
Design: cohort study Participants: 25,186 Evidence: moderate
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Comparisons of ADNC in typical amnestic versus atypical aphasic dementia and of TDP in type A versus type C revealed fundamental biological and clinical differences, suggesting that members of each pair may constitute distinct clinicopathologic entities despite identical downstream proteinopathies. 1 key finding →
Design: longitudinal study Participants: 68 Evidence: moderate
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To develop a new method for measuring Alzheimer's disease (AD)-specific similarity of cortical atrophy patterns at the individual-level, we employed an individual-level machine learning algorithm. 5 key findings →
Design: longitudinal study Participants: 473 Evidence: moderate
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Our results suggest that search strategies that use automated electronic search strategies to extract Charlson comorbidities from the clinical notes contained within the electronic medical record are feasible and reliable. 3 key findings →
Design: cohort study Participants: 1,447 Evidence: moderate
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Changes in the properties of DTI may be the potential mechanism of WMH-related MCI, especially the right IFOF and the right ILF, which may become imaging markers for predicting WMH-related cognitive dysfunction. 2 key findings →
Design: longitudinal study Participants: 22 Evidence: moderate
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We aimed to characterise the brain structure of superagers and identify demographic, lifestyle, and clinical factors associated with this phenotype. 4 key findings →
Design: longitudinal study Participants: 64 Evidence: moderate
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Our results demonstrate that different MAPT mutations give rise to distinct atrophy patterns and clinical phenotype, providing insights into the underlying disease biology and potential utility for patient stratification in therapeutic trials. 3 key findings →
Design: cohort study Evidence: moderate
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Within the training set, individuals closer to or beyond their parent's symptom onset demonstrated reduced grey matter volume and altered functional connectivity, specifically in regions known to be vulnerable in Alzheimer's disease. 5 key findings →
Design: longitudinal study Participants: 138 Evidence: moderate
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The hippocampus is involved at the onset of the neuropathological pathways leading to Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This simple and feasible cognitive impairment prediction model could identify community-dwelling elderly people at the greatest 3-year risk for cognitive impairment, which could help community nurses in the early identification of dementia. 1 key finding →
Design: prospective cohort Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Changes to everyday spoken language ("connected language") are evident in persons with AD dementia, yet little is known about when these changes are first detectable on the continuum of cognitive decline. 2 key findings →
Design: longitudinal study Participants: 264 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.
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 29,780 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →