Of 234 patients, 143 (61.1%) were Aβ-positive. 5 key findings →
Design: cross-sectional Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 234 patients, 143 (61.1%) were Aβ-positive. 5 key findings →
Design: cross-sectional Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The DET framework has achieved superior performance on the classification task across all the evaluation metrics compared to the traditional machine learning based methods, as demonstrated in Table 1. 4 key findings →
Participants: 106 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Regular opioid use was associated with a 20% higher risk of all-cause dementia and a 49% higher risk of vascular dementia (VD) compared with those not using analgesics. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Participants were older adults (mean age 71.5 ± 8.7 years), primarily female (54.2%), and non-Hispanic White (96.5%). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Physical activity was not associated with plasma Aβ42/Aβ40, p-tau217, or brain Aβ burden 7 years later. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In UKB, higher 2-h post-load glucose was associated with a 69% increased Alzheimer's dementia risk (odds ratio 1.69 [95% confidence interval 1.38-2.07]), though this did not replicate in an independent GWAS. 5 key findings →
Participants: 357 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Major systemic diseases elevate AMD risk, compounded by comorbidities. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings revealed a significant impact of unfavorable medical and psychiatric histories on processing speed and visual episodic memory decline (Hazard Ratio (HR) = 1.34, 95% CI: 1.20–1.51, p = 6.06 × 10⁻7; HR = 1.50, 95% CI: 1.22–1.86, p = 1.62 × 10⁻4, respectively). 4 key findings →
Participants: 453,950 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The vast majority of CAA remains sporadic, with increasing prevalence with age and very frequent coexistence with Alzheimer’s disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 is a ubiquitously expressed, primarily nuclear DNA/RNA-binding protein implicated in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 pathology is a hallmark of fatal neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and limbic-predominant age-related TDP-43-encephalopathy (LATE). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We show that TDP-43 activates GSK3 and promotes caspase-dependent cleavage of TDP-43, generating C-terminal fragments. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), highlighted the virus's impact on the central nervous system and its potential to exacerbate neurodegenerative diseases, similar to that in Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Multitarget drugs are molecules with the ability to act simultaneously on different targets at the same time, and they have been evaluated in the last decade as a powerful tool in the development of promising therapeutics for neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Chronic cerebral hypoperfusion (CCH) is a major contributor to vascular dementia, with neuroinflammation playing a central role in its pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Methylglyoxal (MG), a reactive dicarbonyl metabolite associated with diabetes and metabolic disorders, contributes to carbonyl stress, neuroinflammation, and Alzheimer-like neurodegeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral small vessel disease (cSVD) is a common cause of stroke and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dietary high salt intake is increasingly recognized as a risk factor for cognitive decline and dementia, including Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia-mediated neuroinflammation plays a crucial role in memory and cognitive deficits and the development of early mild cognitive impairment (MCI) associated with Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The protein composition of tear fluid (TF) reflects the severity and progression of many age-related diseases. 2 key findings →
Participants: 53 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Five weeks of daily IN dosing of Long Evans rats with 15 μL of a 1% (0.3 mg), but not 0.1% (0.03 mg), solution of DFO rescued cognitive impairment caused by ICV STZ administration as assessed with the Morris Water Maze (MWM) test of spatial memory and learning. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mitochondrial dysfunction plays a preponderant role in the development of Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Most common clinical diagnosis was PSP (41%) for PSP; unspecified FTD (36%) for CBD; AD for AGD (57%) and Other-4R groups (48%), without sex differences. 5 key findings →
Participants: 175 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified several significant sex-specific and sex-dimorphic differentially expressed genes in neurons, microglia, astrocytes and oligodendrocytes, including both cross-sectional changes and alterations from 7 months to 17 months of age. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Emerging evidence suggests that viral infections may contribute to the onset and progression of Alzheimer's disease (AD) and other forms of dementia. 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.
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 →