Nucleocytoplasmic transport defects are observed in Alzheimer's disease (AD) and frontotemporal dementia (FTD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Both LBDs and SPs exhibit distinct visual aberrations, ranging from minor metamorphopsias to complex hallucinations. 5 key findings →
Design: narrative review Evidence: low
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A network neuroscience perspective can significantly advance the understanding of neurodegenerative disorders, particularly frontotemporal dementia (FTD). 5 key findings →
Participants: 28 Evidence: moderate
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We dissociated four key cognitive components underlying remote thinking: spontaneous associative thinking, inhibition of unoriginal responses, intentional remote associative thinking, and verbal initiation; and replicated them in three independent datasets. 5 key findings →
Evidence: low
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Emerging evidence implicating glymphatic dysfunction contributes to the pathogenesis of frontotemporal dementia (FTD). 3 key findings →
Participants: 37 Evidence: low
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could serve as potential biomarkers for NAFLD-associated mild cognitive impairment; 3) bacterial metabolic functions involved in sugar degradation and the breakdown of tryptophan and glutamate were downregulated and linked to CXCL13 plasma levels and neuroinflammation; 4) correlations between SCFA concentrations disappeared with liver disease and cognitive impairment. 3 key findings →
Evidence: low
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Patients with hearing impairment presented slightly altered results on cognitive tests, typical of a mild cognitive impairment. 4 key findings →
Participants: 30 Evidence: low
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Mild cognitive impairment progresses slowly and may be reversible, providing a window of opportunity for intervention before it progresses to Alzheimer's disease, at which point treatments, at best, ameliorate symptoms with little efficacy towards delaying disease progression. 2 key findings →
Evidence: high
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Mild Cognitive Impairment (MCI) is a transitional stage between normal aging and Alzheimer's disease. 5 key findings →
Participants: 476 Evidence: low
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SCD participants were older, had fewer years of education, more depressive symptoms, and more subjective cognitive complaints than CU participants. 4 key findings →
Participants: 315 Evidence: low
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The development of non-pharmacological treatment approaches is supported by evidence that addressing key modifiable risk factors may prevent or delay up to 45% of dementia cases. 5 key findings →
Evidence: low
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Age and years of education (YOE) were identified as independent clinical risk factors for PD-MCI. 5 key findings →
Participants: 1,316 Evidence: low
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A total of 800 questionnaires were sent out in this survey, and 778 were effectively collected, with an effective recovery rate of 97.25%. 5 key findings →
Design: cross-sectional Participants: 82 Evidence: low
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BackgroundStructural changes in medial temporal lobes including the fusiform gyrus, a critical area in face recognition, precede the progression of amnestic mild cognitive impairment (aMCI) to Alzheimer's disease (AD). 2 key findings →
Participants: 32 Evidence: low
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Two distinct subtypes emerged. Subtype 1 (n = 63) features localized supra-normal gray matter volume deviations in dorsolateral prefrontal regions, elevated free water indicating microstructural disruption, executive dysfunction, and transcriptional enrichment in metabolic dysfunction and neurodegenerative pathways. 5 key findings →
Participants: 115 Evidence: moderate
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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
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Only FCSRT-IR LTR rates sufficiently differentiated SCD from HC (AUC of 0.701; 95% CI 0.537-0.865). 4 key findings →
Evidence: low
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Eighteen studies identified four core components of multidomain interventions: physical exercise, cognitive training, nutrition, and cardiovascular risk management. 5 key findings →
Evidence: high
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= 1,217; 65.0 years) showed earlier initial MMSE scores (by 6.1 years, 95% CI = 5.2-7.0), earlier dementia diagnoses (by 2.3 years, 95% CI = 0.9-3.7) but lower dementia risk (adjusted HR = 0.81; 95% CI = 0.69-0.95). 5 key findings →
Evidence: low
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Our findings indicate that the severity of cognitive impairment was significantly associated with an increased risk of falls in patients with dementia. 2 key findings →
Design: cross-sectional Participants: 30 Evidence: low
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Both CDT formats showed clinically useful psychometric properties and similar pragmatic cut‐offs in older psychiatric outpatients. 1 key finding →
Participants: 20 Evidence: low
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anxiety and depression symptoms (HADS), functional autonomy (DAD-6), global cognition (MoCA), and quality of life (WHOQOL). 5 key findings →
Participants: 165 Evidence: low
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40/100
During a median follow-up of 12.8 years, 2219 incident dementias were recorded. 5 key findings →
Participants: 32 Evidence: low
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Flooding has become more frequent and severe worldwide, leading to an increased burden of psychiatric disorders (e.g., depression and anxiety). 5 key findings →
Evidence: moderate
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The relationship between dietary biotin intake and cognitive function remains unclear. 4 key findings →
Participants: 959 Evidence: low
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Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 28,180 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →