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
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
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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
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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
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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
A major hurdle in Alzheimer disease research is the failure of mouse models to capture complexities of the human brain that contributes to repeated clinical trial failure. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A wide range of human diseases are associated with protein misfolding and amyloid aggregates. 2 key findings →
Evidence: low
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It has been demonstrated to have neuroprotective effects in cellular models of neurodegenerative diseases; however, its precise mechanism of action in alleviating tau pathology in Alzheimer's disease (AD), as well as its potential to improve cognitive deficits in animal models, has not yet been elucidated. 3 key findings →
Evidence: low
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The analysis revealed five distinct themes: (1) impact of the program, (2) facilitators enhancing participation, (3) barriers hindering participation, (4) suggestions for improving participation and (5) challenges to adopt digital platforms. 5 key findings →
Evidence: low
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The MI group significantly improved in attention-executive functioning (p = 0.003) compared to ACI (Cohen's d: 0.47, 95% CI 0.13-0.79). 5 key findings →
Evidence: low
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After adjusting for baseline scores via ANCOVA, the experimental group demonstrated significantly higher post-intervention outcomes compared to the control group (p < 0.001). 5 key findings →
Participants: 58 Evidence: low
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Greater perceived control at study baseline was associated with reduced hazard of ADRD. 3 key findings →
Participants: 2,021 Evidence: low
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Mild cognitive impairment in Parkinson's disease (PD-MCI) can affect several cognitive domains, including attention, working memory, executive functions, language, visuospatial skills, and episodic memory, resulting in a progressive reduction of autonomy and an increased risk of dementia. 1 key finding →
Design: clinical trial Participants: 23 Evidence: low
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Although a substantial proportion of TG participants achieved high MI accuracy values, statistical analyses revealed no cognitive improvements specific to TG, suggesting limited efficacy of the MI-based protocol compared to classical cognitive stimulation. 5 key findings →
Evidence: high
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Individuals with Alzheimer’s dementia exhibited poorer nutritional status (EdFED: 8.0 vs. 2.0; NUFFE: 10.0 vs. 7.0; both p < 0.001) and lower adherence to the Mediterranean diet (6.0 vs. 7.0; p = 0.050). 3 key findings →
Participants: 60 Evidence: low
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DSD occurred in 680 patients (39.8%). Compared with dementia alone, DSD was associated with higher PAS scores (5.3 vs. 4.0, p < 0.001), poorer functional status (FIM 48.6 vs. 57.8, p < 0.001) and more frequent in-hospital falls (29.9% vs. 17.5%, p < 0.001). 5 key findings →
Participants: 1,709 Evidence: low
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121 SCU admissions involved 107 unique patients. 5 key findings →
Evidence: low
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Sensor-based surveillance technology (SST) is increasingly employed in the care of people with dementia (PwD) in hospitals, nursing homes, and home care. 1 key finding →
Evidence: low
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The MoCA score and the SCWT duration of the real group improved significantly compared with that of the sham group. 5 key findings →
Participants: 18 Evidence: low
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Up to 60% of people living with dementia who reside in care homes will ‘wander’ at some point. 1 key finding →
Participants: 19 Evidence: low
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Sixteen of 30 cases with DLB pathology had no parkinsonism, which represented diverse nigral neurodegeneration. 5 key findings →
Evidence: moderate
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Caregivers in the control conditions reported significantly worsening sleep efficiency whereas in comparison, those in the active conditions reported improving sleep efficiency. 4 key findings →
Evidence: low
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POD occurred in 43 patients (4.1%). Affected patients were older, in poorer preoperative health, and had longer anaesthesia and surgery times. 5 key findings →
Participants: 43 Evidence: low
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This study included 5899 older adults (65+) of whom 687 reported dysphagia (median age, 80 years; 62.2% female). 5 key findings →
Participants: 5,899 Evidence: low
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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →