28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
The G protein Go is highly expressed in neurons and mediates effects of a group of rhodopsin-like receptors that includes the opioid, alpha2-adrenergic, M2 muscarinic, and somatostatin receptors. 4 key findings →
Evidence: low
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Clinical differential diagnosis of early-onset dementia (EOD) includes familial Alzheimer disease (FAD) and hereditary prion disease. 4 key findings →
Participants: 16 Evidence: low
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Chronic psychological stress is one of the most important triggers and environmental risk factors for neuropsychiatric disorders. 4 key findings →
Evidence: low
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Despite tremendous investments in understanding the complex molecular mechanisms underlying Alzheimer disease (AD), recent clinical trials have failed to show efficacy. 4 key findings →
Evidence: low
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The antemortem diagnosis of Alzheimer disease (AD) requires time-consuming and costly procedures. 4 key findings →
Evidence: low
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TDP-43 is an RNA/DNA-binding protein implicated in transcriptional repression and mRNA processing. 4 key findings →
Evidence: low
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PET of β-Amyloid plaques (Aβ) using [ 18 F ] florbetaben ( [ 18 F ] FBB) and [ 18 F ] fluorodeoxyglucose ( [ 18 F ] FDG) increasingly aid clinicians in early diagnosis of dementia, including Alzheimer's disease (AD), frontotemporal disease, dementia with Lewy bodies, and vascular dementia. 4 key findings →
Participants: 40 Evidence: low
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The study cohort for the analysis of inpatient palliative care comprised 43,896 patients, while the cohort for the analysis of outpatient palliative care included a total of 37,430 patients. 5 key findings →
Participants: 37,430 Evidence: moderate
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Beta-amyloid peptides that are cleaved from the amyloid precursor protein (APP) play a critical role in Alzheimer's disease (AD) pathophysiology. 3 key findings →
Evidence: low
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In October 2019, a Swiss panel of experts met for the Dementia Summit in Brunnen, Switzerland, to discuss the latest scientific findings on basic and clinical research, as well as practical and political approaches to the challenges of dementia disorders in Switzerland. 4 key findings →
Design: longitudinal study Evidence: moderate
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The dual-specific kinase DYRK1A (dual-specificity tyrosine phosphorylation-regulated kinase 1A) is the mammalian orthologue of the Drosophila minibrain (MNB) protein kinase and executes diverse roles in neuronal development and adult brain physiology. 2 key findings →
Evidence: low
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Cognitively impaired patients with negative biomarkers of amyloidosis but with neurochemical evidence of Tau pathophysiology or neurodegeneration or both are classified as "suspected non-Alzheimer pathophysiology" (SNAP), according to the 2018 research framework for a biological definition of Alzheimer's disease (AD). 4 key findings →
Participants: 99 Evidence: low
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The association of Swiss Memory Clinics (SMC) provides intersocietal recommendations for the use of anti-amyloid monoclonal antibodies (mAbs) in Switzerland. 1 key finding →
Evidence: low
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Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are the two most common forms of dementia due to neurodegeneration. 5 key findings →
Evidence: low
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Individual biomarkers significantly predict decline across multiple cognitive domains. 5 key findings →
Evidence: low
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Neuroinflammation is a key feature of Alzheimer’s disease (AD), and stem cell therapies have emerged as promising candidates due to their immunomodulatory properties. 1 key finding →
Evidence: low
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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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The cognitive deficits in Down syndrome (DS) are attributed to an excessive hippocampal inhibition, which obstructs neuronal plasticity and normal learning and memory, a view which is largely based on studies of Ts65Dn mice, the best characterized mouse model of DS. 1 key finding →
Evidence: low
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Neurodegeneration in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) results from both gain of toxicity and loss of normal function of the RNA-binding protein TDP-43, but their mechanistic connection remains unclear. 3 key findings →
Evidence: low
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Forty studies were included. Key stakeholders included healthcare professionals (HCPs); family members and caregivers; PWD; dyads (PWD and their caregivers); the broader public; policymakers; and researchers. 5 key findings →
Evidence: low
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The apolipoprotein E4 (APOE4) variant is the strongest genetic risk factor for Alzheimer disease (AD), while the APOE2 allele is protective. 1 key finding →
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 →