27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
INTRODUCTIONAPOE*{varepsilon}4 is the strongest genetic risk factor for Alzheimers disease (AD), yet its effect varies across ancestral populations. 1 key finding →
Participants: 2,733 Evidence: low
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BackgroundFear of dementia (FoD) can shape psychological well-being and responses to perceived cognitive change. 5 key findings →
Evidence: low
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O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/26361997v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1dac0d9org.highwire.dtl.DTLVardef@aaf8f2org.highwire.dtl.DTLVardef@be10a1org.highwire.dtl.DTLVardef@35c7be_HPS_FORMAT_FIGEXP M_FIG C_FIG BACKGROUNDThe effect of neurovascular health on cardiovascular outcomes is not well-known. 4 key findings →
Participants: 3,263 Evidence: moderate
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IntroductionPolygenic risk scores (PRS) may improve Alzheimers disease (AD) risk prediction before symptom onset, yet choosing an appropriate model can be challenging. 1 key finding →
Evidence: low
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The Middle East and North Africa (MENA) region is projected to experience the fastest growth in dementia burden globally, yet population-based data on cognitive aging remain scarce. 1 key finding →
Participants: 3,027 Evidence: low
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Alzheimers disease (AD) is characterized by substantial clinical and biological heterogeneity, with diverse neuroanatomical, cognitive, clinical, functional, and genetic risk profiles that are poorly captured by current diagnostic frameworks. 4 key findings →
Participants: 393 Evidence: low
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Prior work suggests that perceived value may shape online support use, yet practical and trust-related barriers may still impede uptake even when beliefs are favorable. 5 key findings →
Design: cross-sectional Evidence: low
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In female participants, higher education was associated with lower Thal amyloid phase, diffuse plaques, neuritic plaques, and Braak stage ({beta} range, -0.097 to -0.071; qFDR<.026); none was significant among male participants. 5 key findings →
Design: cohort study Participants: 2,592 Evidence: moderate
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BACKGROUNDSubjective cognitive decline (SCD) may precede mild cognitive impairment (MCI), but not all individuals with SCD progress to MCI. 5 key findings →
Design: longitudinal study Participants: 1,352 Evidence: moderate
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Spatial omics enables the integration of high-dimensional molecular organization with clinical outcomes, yet incorporating spatial single-cell information into predictive models at the population scale remains challenging. 1 key finding →
Evidence: moderate
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Brain iron accumulation is well established in Alzheimers disease (AD), but whether the two share a genetic basis remains unclear. 4 key findings →
Evidence: moderate
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BackgroundAlzheimers disease (AD) pathology often accumulates years before memory loss, creating a need to identify high-risk individuals presymptomatically. 1 key finding →
Evidence: low
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Sex differences in Alzheimers disease (AD) genetic effects and regulatory contexts remain incompletely resolved. 3 key findings →
Participants: 449,335 Evidence: low
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Monoamine oxidase B (MAO-B) is a high-density protein located mainly in astrocytes that influences mitochondrial function and transition to astrogliosis. 2 key findings →
Participants: 13 Evidence: low
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BackgroundDementia is rising worldwide, and in Alzheimer Disease (AD) the loss of communication adds to the burden. 1 key finding →
Evidence: low
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BackgroundDeep-learning models predict mild cognitive impairment (MCI)-to-Alzheimers disease (AD) conversion from structural MRI with high accuracy. 1 key finding →
Design: longitudinal study Participants: 40 Evidence: moderate
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Greater baseline WMH burden was associated with differential longitudinal progression in converters across eleven clinical outcomes, including cognition, gait, and functional independence (all q<0.05). 2 key findings →
Design: longitudinal study Evidence: moderate
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ObjectiveTo determine whether a multi-trait polygenic profile for dementia is associated with dementia- and disability-free survival in middle-aged and older adults. 5 key findings →
Design: longitudinal study Evidence: moderate
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INTRODUCTIONIndividuals with Alzheimers disease (AD) exhibit substantial heterogeneity in the severity of vascular changes and neurodegeneration, making the identification of biologically meaningful subtypes across the AD spectrum critical for improving prognosis and tailoring interventions. 1 key finding →
Design: longitudinal study Participants: 1,396 Evidence: moderate
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Large language models (LLMs) are increasingly used for qualitative analysis, but strong language performance does not guarantee strong interpretation when meaning depends on method and context. 1 key finding →
Evidence: low
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BackgroundTuberous sclerosis complex (TSC) is a rare autosomal dominant neurodevelopmental disorder caused by loss-of-function mutations in TSC1 or TSC2, resulting in chronic hyperactivation of the mechanistic target of rapamycin (mTOR) pathway. 5 key findings →
Evidence: moderate
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BackgroundThe 10 Year Health Plan for England indicates governmental intention to shift care from hospital to community. 1 key finding →
Evidence: low
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BackgroundClonal haematopoiesis (CH), the age-related expansion of mutated blood stem cells, is detectable in around 10% of people in their seventies, rises steeply with age, and is associated with several diseases. 5 key findings →
Design: longitudinal study Participants: 1,091 Evidence: moderate
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BackgroundNon-pharmacological interventions may enhance motor-cognitive integration in prodromal Alzheimers disease (pAD). 5 key findings →
Design: randomized controlled trial Participants: 68 Evidence: high
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Higher education (OR = 1.23, SE = 0.05, 95% CI = [1.10, 1.36], p < 0.001), female sex (OR = 1.30, SE = 0.09, 95% CI = [1.10, 1.55], p = 0.003), and lower age (OR = 0.67, SE = 0.04, 95% CI = [0.61, 0.73], p < 0.001) were associated with increased odds of SuperAger status. 5 key findings →
Participants: 3,513 Evidence: moderate
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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 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.
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 →