27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
BackgroundNeighborhood disadvantage has been associated with reduced cognitive reserve, increased risk for cognitive impairment, and greater Alzheimer's disease (AD) neuropathology, with particularly pronounced effects among Black and Hispanic/Latino older adults. 4 key findings →
Evidence: low
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To determine the relationship between regional brain edema caused by anti-amyloid monoclonal antibody therapy (ARIA-E) and the degree of regional β-amyloid (Aβ) positron emission tomography (PET) signal reduction. 1 key finding →
Evidence: low
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The role of noise pollution as a risk factor for Alzheimer disease (AD) is unclear, with observational studies yielding conflicting results susceptible to confounding and reverse causality. 3 key findings →
Evidence: low
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The onset and sustenance of Alzheimers and Parkinsons is solely dependent on the driving power of the immune cytokine interleukin-1 beta (IL-1β), arising from neuronal distress and release of sAPPα, which activates microglia for synthesis and release of IL-1β driving synthesis of βAPP, Aβ plaques and synthesis and activation of MAPKp38 for phosphorylation of tau for neurofibrillary tangle formation in Alzheimers and for a-synuclein for formation of Lewy bodies in Parkinsons. 1 key finding →
Evidence: low
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Alzheimer disease (AD) is a neurodegenerative disorder characterized by amyloid plaque deposition, neurofibrillary tangles, and chronic neuroinflammation. 3 key findings →
Evidence: low
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Alzheimer disease (AD) is the most common cause of dementia and one of the leading causes of death in adults age 65 y or older in the United States. 1 key finding →
Evidence: low
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Donanemab increased total healthcare costs ($300,689 vs. $178,121) and societal costs ($389,113 vs. $283,618) compared with standard care per capita, while improving health outcomes (4.38 vs. 4.01 QALYs) per capita. 5 key findings →
Evidence: moderate
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The introduction of the first anti-amyloid mAb represents a paradigm shift in the management of AD, but is not free of challenges. 4 key findings →
Evidence: low
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Sowohl in der Tau- als auch in der Amyloid-PET-Bildgebung zeigte die Quantifizierung eine gute bis exzellente Vorhersage der visuellen Beurteilung (Tau: AUC=0,86, p<0,0001; Amyloid: AUC=0,99, p<0,0001). 5 key findings →
Participants: 201 Evidence: low
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Using approximately 5,000 ADNI MRI images, the model achieved 97.67% accuracy, 97.73% precision, 97.67% recall, and 97.65% F1-score, with AUC values near 1.00. 5 key findings →
Evidence: low
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Magnetic Resonance Imaging (MRI) provides detailed structural information, while functional MRI (fMRI) captures temporal brain activity. 2 key findings →
Participants: 29 Evidence: low
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The use of statistical physics models to investigate real-world networks and reveal their underlying dynamics has shown promising results and acquired increasing attention. 2 key findings →
Evidence: low
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How do clinicians distinguish early-stage dementia from the expected cognitive variability seen in ageing adults with Down syndrome? 2 key findings →
Participants: 72 Evidence: low
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Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability. 1 key finding →
Design: narrative review Evidence: low
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For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). 3 key findings →
Evidence: low
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In each case the framework recovered known disease genes and identified biologically coherent, disease-specific modules: in AD, 17 stable high-confidence genes and modules enriched in lipid and cholesterol metabolism and amyloid precursor protein processing; in PD, 17 stable genes and modules associated with mitophagy, ubiquitin-proteasome signaling, and mitochondrial dysfunction; in RA, 20 stable genes and modules enriched in antigen presentation and JAK-STAT cytokine signaling. 2 key findings →
Evidence: low
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Microglia are central regulators of Alzheimer's disease pathogenesis, but their roles cannot be reduced to a simple protective-versus-harmful dichotomy. 4 key findings →
Evidence: low
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Compared with conventional activities, GDRT resulted in significantly greater reductions in overall BPSD (r = 0.56, p = .001) and caregiver burden (r = 0.44, p = .011). 3 key findings →
Evidence: low
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MoCA scores showed significant positive correlations with cognitive-related cerebellar regions, particularly the left Crus I lobule (r = 0.40, p = 0.02) and total Crus I volume (r = 0.36, p = 0.04). 3 key findings →
Evidence: low
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The locus of the gene PTK2B encoding the tyrosine kinase Pyk2 has been associated with the risk of late-onset Alzheimer’s disease, the predominant form of dementia. 3 key findings →
Evidence: low
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In AβO-injected mice, AR, particularly at 200 mg/kg, attenuated memory deficits, reduced hippocampal neuronal degeneration, preserved synaptic protein immunoreactivity and increased markers of hippocampal cell proliferation and immature neurons. 5 key findings →
Evidence: low
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Beyond their role in energy production, mitochondria also interact with other organelles through forming membrane contacts that serve as central hubs of cellular metabolism and signaling. 2 key findings →
Evidence: low
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This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 key findings →
Evidence: low
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Defective mitochondrial quality control is increasingly implicated in tau-mediated neurodegeneration, but how distinct tau lesions in different cell types interact with PINK1-PRKN-mediated mitophagy remains unclear. 4 key findings →
Evidence: low
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To compare and rank the relative and additive effects of lifestyle components including exercise, diet, cognitive training, vascular management, and digital delivery on cognitive outcomes and dementia prevention in older adults without dementia. 1 key finding →
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 →