28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is characterized by the pathological accumulation of amyloid plaques and hyperphosphorylated tau proteins, leading to disruptions in synaptic transmission and neural circuit alterations. 4 key findings →
Evidence: low
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Statistical analysis revealed a trend toward more impaired prefrontal FC with declining cognitive function. 5 key findings →
Evidence: low
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The paper discusses according to prevailing diagnostic systems and algorithms, which cognitive domains that are relevant to investigate, which tests that may be relevant, what kind of norms have satisfactory quality, which cut-off scores do best balance sensitivity and specificity in a neurodiagnostic context, and what kind of conclusions and recommendations that can be drawn from neuropsychological findings. 2 key findings →
Evidence: low
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In the CN group, cerebral microbleed (CMB) progression was associated with the decline in language function (p < 0.05), and deep white matter hyperintensity (WMH) progression was associated with a decline in memory function (p < 0.05). 4 key findings →
Design: longitudinal study Participants: 432 Evidence: moderate
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Mild cognitive impairment (MCI) is an early stage in the progression toward dementia. 1 key finding →
Design: longitudinal study Evidence: moderate
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< 0.0001) were significantly higher for the MCI cohort. 3 key findings →
Design: cohort study Evidence: moderate
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γ-Secretase modulators (GSMs) represent an emerging oral therapy for preventing and targeting Aβ-amyloidosis in Alzheimer disease. 3 key findings →
Evidence: low
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Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer’s disease (AD). 4 key findings →
Evidence: low
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The SorLA protein, encoded by the Sortilin-related receptor 1 ( SORL1 ) gene, is a major player in Alzheimer’s disease (AD) pathophysiology. 4 key findings →
Participants: 30 Evidence: low
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224 subjects progressed to dementia (SCD=38 (9.72%), MCI=186 (50.8%)). 5 key findings →
Participants: 391 Evidence: moderate
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In patients with cognitive impairment due to diverse causes, the HTS might occur regardless of MCI versus dementia status and across different etiologies. 4 key findings →
Participants: 121 Evidence: moderate
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Of 219 completing participants (mean age 73.5 years), the mean SUS score was 82.0 (95% CI: 80.3-83.8), with 84% exceeding the usability threshold (SUS score > 68). 5 key findings →
Participants: 241 Evidence: low
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Data collection began in March 2024. So far 562 people completed a pre-screening online questionnaire, with 190 passing pre-screening of whom 54% met eligibility criteria. 5 key findings →
Participants: 24 Evidence: high
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A total of 64 patients were enrolled in this ongoing real-world study. 5 key findings →
Participants: 64 Evidence: low
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Current metabolomic aging clocks inadequately capture individual heterogeneity in biological aging trajectories, constraining their clinical utility. 4 key findings →
Participants: 196,790 Evidence: low
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Meeting the care needs of people with dementia is a major public health and societal challenge. 1 key finding →
Evidence: low
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Inflammatory responses are characterized by the activation of immune cells, while inflammatory biomarkers intricately interact with the immune system. 4 key findings →
Design: cross-sectional Evidence: moderate
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Except for the visual-spatial memory test, nonlinear approaches provided a better fit than linear methods to model the associations of sedentary time with other cognitive outcomes. 5 key findings →
Participants: 32,875 Evidence: low
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Plasma Aβ 42/40 , p‐tau‐181, and NfL differ in those with CAA and together can discriminate CAA from healthy controls. 4 key findings →
Evidence: low
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Extracellular vesicles (EVs) are membrane-enclosed nanoparticles released by most cell types, and from multiple sub-cellular compartments. 1 key finding →
Evidence: low
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Transactive response (TAR) DNA-binding protein 43 (TDP-43) is a critical RNA/DNA-binding protein involved in various cellular processes, including RNA splicing, transcription regulation, and RNA stability. 1 key finding →
Evidence: low
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TDP-43 protein is an RNA-binding protein linked to amyotrophic lateral sclerosis, frontotemporal dementia, and Alzheimer disease. 1 key finding →
Evidence: low
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The proteinopathy of the RNA-binding protein TDP-43, characterized by nuclear clearance and cytoplasmic inclusion, is a hallmark of multiple neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings were compared to other published RNA sequencing data of tauopathies (Alzheimer's dementia, progressive supranuclear palsy and FTLD with MAPT), FTLD-TDP (subtypes A&B) and available proteomics of this cohort. 5 key findings →
Evidence: moderate
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Fourteen individuals with DS and five age-matched euploid controls were studied, with all DS cases showing HFOs. 5 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 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 →