27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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These findings show that model-based, adaptive assessments can support high-frequency, remote detection and scalable longitudinal monitoring of early memory decline, providing a new way to assess memory decline trajectories in healthy aging and dementia. 3 key findings →
Design: longitudinal study Participants: 24 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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Gross brain findings help guide differential diagnosis, but their diagnostic value across major neurodegenerative diseases remains incompletely characterized. 5 key findings →
Participants: 5,613 Evidence: low
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ObjectivesSubjective word-finding complaints (SWFC) are among the most frequent cognitive complaints in cognitively unimpaired older adults (CU). 3 key findings →
Evidence: moderate
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Plasma biomarkers of amyloid-associated tau phosphorylation (T1) and established tau proteinopathy (T2) can approximate Alzheimers disease stage, but whether plasma-defined stages correspond to broader biological states is unknown. 1 key finding →
Design: cross-sectional Participants: 1,035 Evidence: moderate
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White matter hyperintensities (WMH), a key MRI-marker of cerebral small vessel disease (cSVD), are common in older adults and associated with an increased risk of stroke and dementia. 5 key findings →
Participants: 46,944 Evidence: moderate
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BackgroundBone marrow megakaryocytes, the primary source of brain-derived neurotrophic factor (BDNF) in the blood, secrete BDNF-packed platelets into the bloodstream. 3 key findings →
Design: meta-analysis Evidence: high
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BackgroundLebanon is undergoing substantial demographic and social change, with older adults comprising approximately 10% of the population. 5 key findings →
Design: longitudinal study Participants: 1,871 Evidence: moderate
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IntroductionGenetic studies have shown the APOL1 variant p.N264K, also called M1, is associated with markedly lower kidney disease risk when co-inherited with the G2-risk allele. 4 key findings →
Participants: 40,909 Evidence: low
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--Clinical trajectories after a diagnosis of mild cognitive impairment (MCI) vary widely, so prognostic models must account for both the timing of subsequent diagnoses and unequal follow-up. 2 key findings →
Participants: 401 Evidence: moderate
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It remains unclear whether the combined conditions confer an excess risk of hypoglycaemia-related hospitalisation beyond the risks associated with either condition alone. 5 key findings →
Design: longitudinal study Participants: 329,566 Evidence: moderate
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ImportanceLower relative amplitude of the rest-activity pattern has been associated with cognitive decline and incident dementia in older adults, but its relationship with domain-specific cognitive performance during midlife is less well characterized. 5 key findings →
Design: cross-sectional Participants: 851 Evidence: moderate
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IntroductionRemote cognitive assessments offer an accessible, scalable way to support clinical characterization and longitudinal monitoring of cognition. 3 key findings →
Design: longitudinal study Participants: 209 Evidence: moderate
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INTRODUCTIONDetermining whether plasma biomarkers are preferentially associated with Alzheimers disease (AD)-related rather than age-related brain atrophy patterns may clarify their prognostic and diagnostic clinical use. 5 key findings →
Design: cross-sectional Participants: 818 Evidence: moderate
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ObjectiveTo externally replicate and extend prior findings across two structurally independent healthcare data sources, evaluating whether predominant use of antihypertensive medications that stimulate versus inhibit angiotensin II type 2 and type 4 receptor signaling is associated with risk of incident ADRD. 4 key findings →
Design: cohort study Participants: 1,596,034 Evidence: high
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Neuroinflammation is a principal driver of brain atrophy and cognitive decline in Alzheimers disease (AD). 2 key findings →
Participants: 49 Evidence: low
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INTRODUCTIONSleep-dependent memory consolidation is impaired early in Alzheimers disease (AD). 2 key findings →
Participants: 37 Evidence: high
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ImportanceAnxiety phenotypes - rumination, global anxiety, and worry (RAW) - are increasingly associated with Alzheimers disease and related dementias (ADRD) risk, yet how anxiety phenotypes relate to coordinated, multi-system biology in the at-risk older adults is unknown. 4 key findings →
Design: longitudinal study Evidence: moderate
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Alzheimers disease and related dementias (ADRD)1 and Parkinsons disease and related disorders (PDRD)2 have substantial genetic contributions, yet the role of rare damaging coding variants remains incompletely characterized at population scale3-6. 1 key finding →
Evidence: low
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Structured AbstractO_ST_ABSBackgroundC_ST_ABSThe genetic architecture of Alzheimer disease remains incompletely understood. 2 key findings →
Evidence: low
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 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 →