We identified 471 proteins with significant interaction effects between T2D and dementia risk. 5 key findings →
Participants: 2,920 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We identified 471 proteins with significant interaction effects between T2D and dementia risk. 5 key findings →
Participants: 2,920 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Advanced atherosclerosis is the pathological basis for acute cardiovascular events, with significant residual risk of recurrent clinical events despite contemporary treatment. 4 key findings →
Evidence: low
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By 2060, ADRD cases in China are projected to reach approximately 49.89 million, with the highest prevalence and economic burden concentrated in provinces such as Shandong, Sichuan, Jiangsu, Henan, and Guangdong. 5 key findings →
Design: longitudinal study Evidence: moderate
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This longitudinal evidence supports a link between the ALPS-I and cognitive degeneration. 3 key findings →
Design: longitudinal study Evidence: moderate
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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
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A significant median Centiloid reduction of 30.9 was observed, with a 24.1% amyloid PET negativity rate after six months. 3 key findings →
Participants: 42 Evidence: moderate
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The rising incidence of Alzheimer's disease (AD) poses significant challenges to traditional diagnostic methods, which primarily rely on neuropsychological assessments and brain MRIs. 2 key findings →
Evidence: low
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There are many reports about the comorbidity of NPH and other neurodegenerative diseases1–3; the primary findings in neuropathological studies of patients with NPH include amyloid plaques and hyperphosphorylated tau protein inclusions.2,4 This suggests that proteinopathy may be one of the potential causes of NPH. 5 key findings →
Design: cohort study Participants: 50 Evidence: moderate
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=0.002). Early-onset CHD and genetic susceptibility are associated with a higher risk of incident dementia and a larger WMH volume. 2 key findings →
Design: cohort study Participants: 671 Evidence: moderate
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Oral diseases have emerged as one of the most prevalent non-communicable diseases (NCDs) worldwide, with a high global average prevalence of 45%, affecting an estimated 3.5 billion people globally. 1 key finding →
Evidence: low
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Of 289,649 included participants, 137,480 (47.5 %) were male, and the mean age was 56.6 ± 8.1 years. 5 key findings →
Design: cohort study Evidence: moderate
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Cancer is a leading cause of death in China, and its epidemiological profile has shifted markedly in recent years. 5 key findings →
Evidence: low
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Higher FBG level at midlife was not associated with an increased risk of dementia. 5 key findings →
Evidence: moderate
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With a rapidly aging population, general practitioners are confronting the challenge of how to determine those who are at greatest risk for dementia and potentially need more specialized follow-up to mitigate symptoms early in its course. 4 key findings →
Evidence: low
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Progranulin haploinsufficiency causes frontotemporal dementia with tau-negative, ubiquitin-positive neuronal inclusion pathology. 4 key findings →
Evidence: low
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BackgroundElectroencephalogram (EEG) is a promising, non-invasive method for identifying the presence of Alzheimer's disease (AD) by recognizing specific brain activity patterns associated with the disease. 3 key findings →
Participants: 431 Evidence: low
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Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear. 4 key findings →
Evidence: low
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Among the 116 patients studied, 62.1% exhibited effective responses, 12.1% showed ineffectiveness, and 25.9% had uncertain outcomes with valproate therapy. 5 key findings →
Participants: 116 Evidence: high
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In 2021, the age-standardised rates for ADOD were 694.01 (95% uncertainty intervals [UIs]: 602.88 to 794.08) for prevalence, 119.76 (95% UI: 104.96 to 135.89) for incidence, and 481.70 (95% UI: 228.79 to 1,023.96) for disability-adjusted life years (DALYs). 5 key findings →
Evidence: moderate
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A total of 156 patients were clinically diagnosed with dementia based on the 2011 NIA-AA criteria, regardless of specific disease etiology, and all exhibited significant brain atrophy on anatomical magnetic resonance imaging (MRI), indicating neuronal injury (N+). 5 key findings →
Participants: 156 Evidence: moderate
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Over a median follow-up of 3.26 years, 321 participants converted to AD. 5 key findings →
Participants: 762 Evidence: low
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Naodesheng (NDS) formula, which consists of Rhizoma Chuanxiong, Lobed Kudzuvine, Carthamus tinctorius, Radix Notoginseng, and Crataegus pinnatifida, is widely applied for the treatment of cardio/cerebrovascular ischemic diseases, ischemic stroke, and sequelae of cerebral hemorrhage, etc. At present, the studies on NDS formula for Alzheimer's disease (AD) only focus on single component of this prescription, and there is no report about the synergistic mechanism of the constituents in NDS formula for the potential treatment of dementia. 5 key findings →
Evidence: low
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What is already known about this topic?: As the Chinese population ages, the prevalence of cognitive impairment among older adults continues to increase. 1 key finding →
Evidence: low
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-glycans found at the N304 site of lecanemab of the heavy chain. 1 key finding →
Evidence: low
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The pathological activation of AD microglia significantly amplifies endogenous aging characteristics. 4 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →