30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
H. cheirifolia phenolic extracts exhibit potent, mechanism-specific antioxidant activity and promising AChE inhibition, validating traditional use in neurological complaints. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A bstract INTRODUCTION Treatment response in Alzheimer’s disease (AD) varies substantially across patients, yet no validated frameworks exist to estimate heterogeneous treatment effects (HTE) from observational data while controlling for confounding bias. 2 key findings →
Participants: 4,049 Evidence: low
Full summary, score breakdown and related studies → Original source
2.1 Case İnformation A 78 years old man was referred to the cardiology clinic because of mild dyspnea. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
High placebo response is an obstacle in developing drugs to treat agitation in Alzheimer’s disease (AAD), a prevalent and burdensome symptom. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings confirm the diagnostic value of urinary β-amyloid protein detection in MCI and AD-related dementia. 5 key findings →
Design: case-control study Participants: 51,187 Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease is increasingly linked to metabolic dysfunction, with insulin resistance emerging as a key contributor to tau pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Severe cognitive decline due to dementia is an important clinical indicator signaling neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) are central regulators of synaptic homeostasis, plasticity, and dysfunction during Alzheimer’s disease (AD) progression. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) remains one of the most devastating and economically costly neurological conditions of the modern era, affecting over 55 million individuals worldwide with no approved disease-modifying therapy. 3 key findings →
Participants: 1,348 Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases are a major threat to older adults and represent a growing global health burden as the elderly population continues to expand. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
IKZF1 is prioritised as a candidate late-disease microglial TF, supported by six convergent evidence dimensions including independent bulk replication. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
STRUCTURED ABSTRACT INTRODUCTION This study examined the extent to which educational attainment, Alzheimer’s disease (AD) knowledge, and research attitudes are associated with willingness to participate in AD research, and whether AD knowledge and research attitudes mediate associations between educational attainment and willingness to participate. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Insomnia disorder affects approximately 10–20% of adults and is usually chronic. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Sleep disturbance in Alzheimer’s disease (AD), particularly the reduction of slow wave sleep (SWS), has been proposed as a novel therapeutic target, with disease-modifying potential. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Controlling for baseline differences, treatment of OSA improved delayed recall and may reduce the slope of memory decline in Alzheimer’s disease and vascular dementia. 3 key findings →
Design: cohort study Participants: 86 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The glycolytic regulator PFKFB3 supports dysfunctional β-cell states, but its role in pancreatic Ca 2+ signaling remains unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular dementia (VaD) is a leading cause of cognitive decline with no disease-modifying therapies. 2 key findings →
Participants: 437,749 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that cognitive impairment may mark a population vulnerable to medication complexity rather than independently driving DDI risk, with polypharmacy emerging as the principal modifiable determinant. 4 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
Cortisol is primarily synthesized by the adrenal glands, but also within specific tissues via a distinct enzymatic pathway. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyses the synthesis of cortisol within cells to create local higher cortisol environments in those organs where it is highly expressed such as the liver and brain. 4 key findings →
Participants: 247 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings identify restoration of hippocampal transcript fate and splice-isoform selection as a mechanism potentially underlying A. muciniphila -mediated protection against Cd neurotoxicity, and establish post-transcriptional RNA regulation as a gut-brain target for mitigating environmentally driven neurotoxicity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Air pollution (AirP) exposure is associated with increased Alzheimer’s disease (AD) risk, yet AirP is chemically heterogeneous, complicating identification of shared pathogenic drivers. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
FDA-approved carbonic anhydrase inhibitors (CAIs) have shown robust efficacy in reducing amyloid-β (Aβ) pathology, neurodegeneration, and cerebrovascular dysfunction in Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA) models, highlighting carbonic anhydrase (CAs) as a promising, previously untapped therapeutic target for AD and vascular contribution to dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
VU0155069 engages circuit- and pathological stage-specific forms of dendritic spine remodeling across distributed recognition- and associative-memory networks. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a widely prevalent neurodegenerative disorder characterized by progressive cognitive impairment and neuropathological alterations. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
More than one-quarter of residents with ADRD remain untreated with guideline-recommended pharmacotherapy, and treatment varied significantly by non-clinical predictors. 5 key findings →
Participants: 359,801 Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 3,607 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 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