27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
During a median follow-up of 13.68 years, 4744 incident all-cause dementia (ACD) events (including 3013 Alzheimer's disease (AD) and 853 vascular dementia (VaD)) were recorded. 5 key findings →
Participants: 846 Evidence: low
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Both the higher parental dementia instrument and participant genetic instrument score were associated with higher mean SBP (difference in mean SBP mmHg per 1SD higher score: 0.12, 95% CI 0.06 to 0.17, p < 0.0001, and 0.07, 95% CI 0.00 to 0.13, p=0.037, respectively) but not DBP. 5 key findings →
Participants: 501,420 Evidence: low
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This study examined the proteome associated with TDP-43 inclusions in ALS, using mass spectrometry-based proteomic analysis of spinal cord and cerebral cortex from donors with phosphoTDP-43 positive ALS (n = 16), alpha-synuclein positive Parkinson's disease (PD, n = 8), phosphotau and beta-amyloid positive Alzheimer's disease (AD, n = 8) and age matched non-neurological controls (n = 8), comparing ALS with non-ALS conditions, spinal cord with cerebral cortex samples, and detergent-soluble with -insoluble fractions. 5 key findings →
Participants: 16 Evidence: low
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Among 1,307 individuals, 36.9% were non-White and 49.7% were women. 5 key findings →
Participants: 432 Evidence: low
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TDP-linked proteinopathies, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and limbic-predominant age-related TDP-43 encephalopathy (LATE), are characterised by pathogenic deposits containing transactive response DNA-binding protein 43 (TDP-43) in the brain and spinal cord of patients. 1 key finding →
Evidence: low
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Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear. 4 key findings →
Evidence: low
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We identified 34 epidemiological studies that met the inclusion criteria. 5 key findings →
Design: narrative review Evidence: low
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Copy number variation (CNV) of the amyloid-β precursor protein gene (APP) is a known cause of autosomal dominant Alzheimer disease (ADAD), but de novo genetic variants causing ADAD are rare. 2 key findings →
Evidence: low
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Recent reports suggest dysregulation of the N6-methyladenosine (m6A) RNA modification may contribute to the pathology of neurodegenerative diseases. 4 key findings →
Evidence: low
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The concomitant depletion of dopaminergic and serotonergic inputs within the hippocampus of C57BL/6N mice provokes a pronounced activation of microglia via the NLRP3-inflammasome pathway, accompanied by increased IL-1β expression. 5 key findings →
Evidence: moderate
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Mitochondrial oxidative stress and neuroinflammation are involved in the onset and progression of Alzheimer's disease (AD). 5 key findings →
Evidence: low
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In PD patients, a decrease in [ 18 F]DOPA PET retention correlated with disease duration as well as CSF neurodegenerative and synaptic biomarkers but not with inflammatory biomarkers or [ 18 F]RO948 PET midbrain off-target retention. 2 key findings →
Participants: 623 Evidence: low
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Tauopathies are neurodegenerative diseases characterized by pathological tau protein inclusions and dementia. 5 key findings →
Evidence: low
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Metabolic syndrome markers, such as insulin resistance and the triglyceride/HDL C ratio, correlate with early cognitive impairment. 5 key findings →
Evidence: moderate
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Our findings revealed significantly elevated CSF GAP-43 levels in individuals with AD compared to CN and MCI groups. 4 key findings →
Participants: 1,639 Evidence: moderate
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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss and cognitive decline, with women being disproportionately affected in both prevalence and severity. 1 key finding →
Evidence: low
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LLMD participants were more likely to be tau PET and Aβ PET positive than HCs. 5 key findings →
Evidence: low
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At baseline, MCI participants displayed elevated levels of IL-17A, CX3CL1, CCL11, with a borderline increase of IL-6 and TNFα. 5 key findings →
Participants: 76 Evidence: low
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To date, the impact of cognitive therapies on patients with dementia and mild cognitive impairment (MCI) has been studied in terms of cognition, quality of life and activities of daily living rather than in the context of neuropsychiatric symptoms (NPS). 5 key findings →
Participants: 4,089 Evidence: low
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Participants numbered 3334 and had a median age of 62 years. 5 key findings →
Design: cohort study Evidence: moderate
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Higher general burden was associated with female caregivers (β = −.19, p = .05), higher education (β = .16, p = .03), caring for someone with dementia (β = .36, p = .01), and greater dysphagia-related burden (β = .33, p = .01). 5 key findings →
Participants: 211 Evidence: low
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= 18 556) lived in care homes before death. 4 key findings →
Design: cohort study Evidence: moderate
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The statistical analysis revealed that the survival time was significantly longer in females compared to males (p = 0.003). 5 key findings →
Design: cohort study Participants: 54 Evidence: moderate
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Genetic variants increase the risk of neurocognitive disorders in later life, including vascular dementia (VaD) and Alzheimer’s disease (AD), but the precise relationships between genetic risk factors and underlying disease etiologies are not well understood. 4 key findings →
Evidence: low
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Amyloid status moderated associations between IIV-dispersion and WMH, such that higher IIV-dispersion was associated with greater WMH in Aß+ individuals whether WMH was examined as a continuous (B = 0.30, ß = 0.13, p = .006) or a dichotomous variable based on quartiles (odds ratio [OR] = 2.41, p < .001). 4 key findings →
Participants: 819 Evidence: low
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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. 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 →