30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 822 individuals enrolled in the HEAD study, 681 participants spanning cognitively unimpaired to dementia were included. 5 key findings →
Design: cross-sectional Participants: 681 Evidence: moderate
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Critical appraisal will not be undertaken, as it is optional in scoping reviews and is not aligned with the primary mapping objectives of this review. 5 key findings →
Design: meta-analysis Evidence: high
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There were 56.9 million people worldwide living with dementia in 2021, according to the Global Burden of Disease study, and this number is projected to exceed 137 million by 2050. 1 key finding →
Evidence: low
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In MCI and dementia, the HTS is an ecologically valid non-canonical sign, frequently occurs in daily life too, associated with longer disease duration and spatial disorientation. 2 key findings →
Design: retrospective cohort Participants: 71 Evidence: moderate
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Routine liver–metabolic indices were associated with cognitive performance, while FIB-4 stage showed effect modification by APOE ε4 in relation to both cognition and amyloid PET SUVR. 4 key findings →
Design: longitudinal study Participants: 507 Evidence: moderate
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In the ADMET2 biomarker subset (n = 44, MPH:21, age:75 years, MMSE:20.2), higher baseline TNF was associated with higher M6 NPI-A [B(SE)= 6.86 (1.71), p = .0003], and multivariable models found lower baseline TNF [B(SE)= 8.28(1.61), p < .001] and higher baseline S100B [B(SE)= -6.41(1.95), p = .002] were associated with lower M6 NPI-A. Exploratory analyses suggested that higher baseline NfL significantly interacted with treatment to predict lower M6 NPI-A [B(SE)= -8.36(4.21), p = .05], only when adjusting for cognition. 5 key findings →
Participants: 44 Evidence: high
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Shorter LTL was associated with an increased risk of NDDs, including Alzheimer's disease (HR: 0.52, 95% CI 0.40-0.67, P < 0.001), dementia in AD (HR: 0.53, 95% CI 0.39-0.73, P < 0.001), unspecified dementia (HR: 0.74, 95% CI 0.58-0.95, P < 0.05), degenerative diseases of the nervous system (including other specified degenerative diseases such as circumscribed brain atrophy and senile degeneration of the brain) (HR: 0.62, 95% CI 0.45-0.84, P < 0.01), extrapyramidal and movement disorders (including other specified extrapyramidal and movement disorders such as a range of tremors, chorea, tics, and other abnormal involuntary movements) (HR: 0.63, 95% CI 0.48-0.82, P < 0.01), and mental and behavioral disorders due to use of alcohol (HR: 0.46, 95% CI 0.38-0.55, P < 0.001). 5 key findings →
Participants: 459,902 Evidence: moderate
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Using human stem cell-derived neurons, we show that TDP-43 reduction induces cryptic splicing and downregulation of these genes, resulting in impaired excitability and synaptic transmission. 1 key finding →
Evidence: low
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The study describes 4 males who developed dementia following confirmed or suspected c-hGH treatment in childhood (age at symptom onset between 47 and 60 years) with cognitive syndromes characterized by prominent language involvement. 4 key findings →
Participants: 14 Evidence: low
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Microglia are implicated in the progression of Alzheimer's disease (AD) pathology from its earliest stages, suggesting that cerebrospinal fluid (CSF) microglia profiling across clinical AD stages can aid in treatment development and monitoring. 3 key findings →
Participants: 834 Evidence: low
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Cognitive training produced a significant, moderate improvement in cognitive task performance (Hedges’ g = 0.451, 95% CI 0.207–0.696; p < .001). 5 key findings →
Design: meta-analysis Evidence: high
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VLAHE residents had fewer hospitalizations and shorter stays (10.5 vs 15.2 days, P = .0004) than comparable NH residents, particularly for acute care. 5 key findings →
Design: longitudinal study Evidence: moderate
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Considerable data support the presence of both systemic and CNS inflammation in SVD and VCID. 3 key findings →
Design: longitudinal study Evidence: moderate
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Early and accurate detection of Alzheimer's disease (AD) is essential for timely intervention and development of disease-modifying treatments. 1 key finding →
Design: longitudinal study Evidence: moderate
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Alzheimer disease (AD) risk differs across ancestral populations, yet most genetic studies have focused on non-Hispanic White (NHW) cohorts. 1 key finding →
Design: cross-sectional Participants: 751 Evidence: early
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HRU and payments were overall similar between A4 and LEARN Medicare. 5 key findings →
Design: cohort Participants: 367 Evidence: early
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
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The study cohort included 1 415 265 long-stay nursing home residents with dementia who died between 2013 and 2022. 5 key findings →
Design: cohort study Evidence: moderate
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This cohort study examines the association of serum hyperphosphorylated tau and neurofilament light chain concentrations with psychosis in Alzheimer disease. 1 key finding →
Design: cohort study Evidence: moderate
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In their study, Chen et al 1 examined the association between apolipoprotein E (APOE) genotype and longitudinal cognitive trajectories among middle-aged and older East Asian adults participating in the Healthy Aging Longitudinal Study of Taiwan (HALST).Although sporadic late-onset Alzheimer disease (AD) is polygenic, APOE remains the strongest genetic determinant of AD risk, with carriers of the APOE ε4 allele having increased odds of developing AD dementia in a dose-dependent manner compared with APOE ε3 homozygotes. 1 key finding →
Design: longitudinal study Participants: 21 Evidence: moderate
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Three trajectory classes were identified: stable, slow decliners, and fast decliners. 4 key findings →
Design: longitudinal study Evidence: moderate
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Four thousand four hundred eighty-six participants were included (mean age 71.3 ± 4.7 years, 30% participants Aβ+, 59% female). 5 key findings →
Design: cross-sectional Evidence: moderate
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Dementia research often suffers from methodological pitfalls such as label-information and subject-information leakages. 2 key findings →
Design: longitudinal study Evidence: moderate
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Lower SES and education were the strongest predictors of increased behavioral risk. 5 key findings →
Design: cross-sectional Participants: 1,730 Evidence: low
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Isolated rapid eye movement sleep behavior disorder (iRBD) is a major prodromal marker of α-synucleinopathies, often preceding the clinical onset of Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy. 3 key findings →
Participants: 31 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events