27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 70 autopsied individuals (62 male, 8 female; mean [SD] age, 64.40 [13.94] years), 20 showed CTE-NC in the brain. 5 key findings →
Design: case-control study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
UNDERLYING BIOLOGICAL MECHANISMS PNDs result from a complex interplay of multiple biological, genetic, and environmental factors (Table 1). 5 key findings →
Design: systematic review Participants: 7,900 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The Dominantly Inherited Alzheimer Network Observational Study (DIAN Obs) is a longitudinal, global cohort study investigating brain aging and autosomal dominant Alzheimer’s disease (ADAD), a rare monogenic form of Alzheimer’s disease (AD). 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2) is a key immunomodulatory receptor broadly expressed on myeloid cells such as macrophages and microglia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Female Psen1 mutation(L166P) mice were found to have reductions in whole-body mineral density (BMD) and bone mineral content as early as one month and a sustained bone phenotype with age with loss in cortical and trabecular properties compared to age-and gendermatched wildtype control mice, whereas male mice did not (Fig.1A-C). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Perspectivas futuras O mesmo princípio de modulação glial pode ser aplicado em cenários de morte clínica (parada cardiorrespiratória). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This diploma thesis presents the work carried out during 6 months within the Laboratory directed by Professor Millet, written under the supervision and with the support of Dr. Benjamin Tournier and Silvia Braconi Quintaje. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) affects over 55 million people worldwide and lacks effective disease-modifying therapies targeting neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We report the results of structural, functional and genetic studies on the CD33 sialic acid- binding receptor that reveal how non-coding variants in CD33 alter risk for Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid precursor protein (APP) is a key player in various neuronal functions but also the source for toxic Aβ that accumulates in the brain of Alzheimer patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Key recommendations emphasize that tissue biopsies remain essential for amyloidosis diagnosis and typing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APP‐mediated signaling plays a key role in regulating sleep, maintaining BBB integrity, and preserving memory in AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found a moderate yet significant reduction in Aβ plaque size in male 5×FAD × mAPPA673T compared with 5×FAD mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive and complicated neurodegenerative disorder that mostly affects the elderly and is characterized by memory loss, cognitive dysfunction, accumulation of amyloid beta (Aβ) plaques, neurofibrillary tangles, and cholinergic deficits. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
The pathological activation of AD microglia significantly amplifies endogenous aging characteristics. 4 key findings →
Evidence: low
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HIIT alone and in combination with CBD treatment significantly improved cognitive impairment induced by AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The review further discusses AI-driven nanomedicine optimization and advanced human-relevant models, including brain-on-a-chip systems and three-dimensional (3D) bioprinting, as tools to improve translational prediction. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Perspectivas futuras O mesmo princípio de modulação glial pode ser aplicado em cenários de morte clínica (parada cardiorrespiratória). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This diploma thesis presents the work carried out during 6 months within the Laboratory directed by Professor Millet, written under the supervision and with the support of Dr. Benjamin Tournier and Silvia Braconi Quintaje. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Introducción. La enfermedad de Alzheimer (EA) es una condición neurodegenerativa progresiva caracterizada por el deterioro cognitivo, la acumulación de beta-amiloide y la neuroinflamación. La tecnología CRISPR/Cas9 ha emergido como una herramienta prometedora para investigar y, potencialmente, tratar la EA, permitiendo ediciones precisas del genoma y la modulación de la expresión génica. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) affects over 55 million people worldwide and lacks effective disease-modifying therapies targeting neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mechanistic studies demonstrate that pharmacological modulation of microglial phenotypes inhibition of pro inflammatory mediators TNF alpha IL 1 IL 6 and targeting pathways such as NF kappa B NLRP3 inflammasome p38 MAPK JAK STAT and TREM2 can attenuate neuroinflammatory cascades and reduce amyloid beta and tau associated neurotoxicity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dysregulated ferritinophagy-mediated ferroptosis is a pivotal AD pathogenic target. 5 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 →