Physiological pulsations maintaining brain neurofluidic homeostasis are altered early in the course of Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Physiological pulsations maintaining brain neurofluidic homeostasis are altered early in the course of Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Four main themes were extracted: (1) Positive experiences, including perceived improvement in cognitive function and mood; (2) Facilitators and barriers to training participation, with facilitators comprising dementia care experience, higher educational attainment, and availability of free time, and barriers including unfamiliarity with computer operation, low awareness of cognitive training, and lengthy training sessions; (3) Training content preferences, reflecting a desire for both relaxed, engaging content and professional guidance; and (4) Practical dilemmas and suggestions, including difficulties in understanding task instructions and complex login procedures, with recommendations for detailed task descriptions and simplified procedures. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although smartphone usage time is not directly associated with ikigai in older adults, it may reflect preserved physical and cognitive abilities required to navigate digital environments. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
This study provides quantitative evidence supporting the complementary use of multiple cognitive assessment tools. 4 key findings →
Design: cross-sectional Participants: 250 Evidence: low
Full summary, score breakdown and related studies → Original source
Our study delivers ambivalent results for the efficacy of care management for caregivers. 3 key findings →
Design: randomized controlled trial Participants: 96 Evidence: high
Full summary, score breakdown and related studies → Original source
Although most Korean older adults declined LST regardless of living arrangement, determinants of LST preferences differed according to household structure. 5 key findings →
Design: longitudinal study Participants: 3,787 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Ignite is a sensitive digital cognitive assessment capable of detecting early cognitive changes in genetic FTD and demonstrates improved discrimination compared with standard neuropsychological measures at milder disease severity. 5 key findings →
Participants: 190 Evidence: low
Full summary, score breakdown and related studies → Original source
Structured metabolic genetic axes reveal selective and biologically distinct links between circulating metabolism and neurodegenerative disease, providing a framework for mechanism-focused follow-up beyond single-metabolite association. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the present analysis, genetic risk and end-stage AD pathology are largely decoupled at the level of individual genes and pathways but converge on a shared, pharmacologically modifiable response landscape. 1 key finding →
Participants: 3,202 Evidence: low
Full summary, score breakdown and related studies → Original source
Genetically predicted BP raises WMH in European and Japanese ancestry. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inverse-variance weighted MR indicated that genetically predicted focal epilepsy with hippocampal sclerosis was associated with increased odds of AD (OR=3.99, 95% CI 1.17–13.61; P=0.027). 5 key findings →
Participants: 803 Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic pain and cognitive impairment are rising ageing-related burdens. 4 key findings →
Design: longitudinal study Participants: 387,649 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuronal activity must be tightly controlled to maintain brain function. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Truncated tau is increasingly recognized as a pivotal pathogenic event in Alzheimer’s disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
EA ameliorated cognitive impairment in APP/PS1 mice by enhancing TREM2⁺ microglia-mediated Aβ clearance and suppressing neuroinflammation. scRNA-seq further revealed that EA reshaped microglial transcriptional states and intercellular communication networks in a TREM2-dependent manner. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These data further support the use of the LOAD2.Mthfr 677C>T mouse model to study aspects of ADRD such as cerebrovascular compromise. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is characterized by marked biological heterogeneity, only partly explained by the frequent presence of Alzheimer’s disease (AD) copathology. 4 key findings →
Design: longitudinal study Participants: 129 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) disproportionately affects women, who exhibit greater vulnerability to Tau pathology and neuroinflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Based on the exacerbated AD pathological features and transcriptomic alterations observed in Arf4 knockdown animals, ARF4 appears to play a critical role in AD resilience and may represent a potential prognostic factor worthy of further investigation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Realising PCC in YOD requires not only identifying individual needs and appropriate care components, but also ongoing alignment of changing needs, expectations, timing, and responsibilities across the care trajectory. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
2µM FAM labelled β-amyloid 1–40 was transported through CLEFF4 cells with an apparent permeability (Papp) of 4.47x10 − 6 cm/sec in the efflux direction (Basolateral (Bas) to apical (Ap)) while Ap to Bas direction was only 1.67x10 − 6 cm/sec. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Active PTB was associated with widespread transcriptional remodeling, with 1,389 dysregulated genes organized into 16 PTB-associated co-expression modules. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a progressively characterized neurodegenerative condition marked by molecular instability, neuronal dysfunction and abnormal tau buildup. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although Alzheimer’s disease (AD) and glioblastoma (GBM) share common aging-related risk factors, they lead to opposite cellular fates—neurodegeneration versus uncontrolled proliferation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Computational drug repurposing commonly relies on transcriptomic signature matching to identify compounds that reverse disease-associated gene expression, but such approaches do not distinguish putative causal drivers from downstream consequences of disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →