Risk of Alzheimer disease is increased in patients with diabetes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Risk of Alzheimer disease is increased in patients with diabetes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This article addresses the potential legal ramifications for neurologists caring for patients with Alzheimer disease (AD) who elect neither to prescribe aducanumab nor to refer patients with AD for treatment with aducanumab. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Our findings reveal various concerns about Aduhelm involving efficacy, safety, and affordability. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a neurodegenerative disorder whose etiology continues to be discussed, to the point that there are different hypotheses that seek to clarify it, in addition to the fact that, given its multifactorial nature, there are different risk factors associated with its development. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
On June 7, 2021, the US Food and Drug Administration (FDA) approved aducanumab, a monoclonal amyloid targeting β-amyloid, for the treatment for Alzheimer's disease (AD). 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Various medicinal agents aimed at improving Alzheimer disease (AD) include cholinesterase inhibitors, memantine, aducanumab, and antioxidants. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The recent approval of aduhelm/aducanumab by the US Food and Drug Administration (FDA) in June 2021 raised hopes that further substances against Alzheimer's disease might be approved in the near future. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BSA-polymer conjugates displayed enhanced resistance to proteolytic degradation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The author panel systematically reviewed available clinical trial data detailing aducanumab use in individuals with early symptomatic Alzheimer disease. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We estimated associations of educational attainment and Alzheimer disease genetic risk with treatment initiation and incident dementia and compared GLP-1 receptor agonist initiators with initiators of non-sodium-glucose cotransporter 2 inhibitor second-line therapies, with a separate sodium-glucose cotransporter 2 inhibitor compa 4 key findings →
Design: cohort study Participants: 14,364 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E). 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Therapies targeting amyloid, such as monoclonal antibodies like Lecanemab, Aducanumab, and Donanemab, have garnered FDA approval but remain controversial due to limited clinical benefits and significant side effects against Alzheimer. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent clinical and epidemiological studies support the contention that diabetes mellitus (DM) is a strong risk factor for the development of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) is an RNA-binding protein that mislocalizes to the cytoplasm and forms stress-induced granules in tauopathy and multisystem proteinopathy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated protein tau is an intrinsically disordered protein (IDP) that forms characteristic fibrillar aggregates in several diseases, the most well-known of which is Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Haploinsufficiency of progranulin (resulting from mutations in the GRN gene) is a major genetic cause of frontotemporal dementia (FTD), which is characterized by profound changes in personality and behavior, progressive impairments in executive function, speech, language and/or movement, TDP-43 pathology, lysosomal dysfunction, and neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Electrochemical biosensors offer a promising route for the rapid, non-invasive detection of disease biomarkers by converting biochemical interactions into measurable electrical signals. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings shift AD modeling from passive proteotoxicity to an active, misregulated developmental structural engine, offering a mechanical framework that explains early olfactory vulnerability and non-linear anti-tau clinical trial responses. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Long non-coding RNAs (lncRNAs) are increasingly recognized as regulators of brain cell function, but their roles in astrocyte biology and neurodegeneration remain poorly understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aberrant alternative splicing alters multiple disease-associated splicing events, including MAPT exon 10 inclusion linked to tau pathology, and thereby impacts Alzheimer’s disease (AD) progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulation of tau tangles and Aβ plaques are prominent neuropathologies that characterize Alzheimer’s disease (AD) and Down Syndrome (DS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by abnormal aggregation of the tau protein. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and Down Syndrome (DS) are characterized by the aggregation of tau tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer’s disease (AD) and related tauopathies, progressive pathology has been linked to prion mechanisms whereby ordered tau assemblies, or “seeds,” form in one cell and transit to neighboring or connected cells where they serve as templates for their own replication. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma pTau-181 demonstrates flat or declining longitudinal trajectories and minimal cognitive correlation, suggesting tau is a static biomarker rather than a dynamic therapeutic target in mid-to-late adulthood. 2 key findings →
Design: cross-sectional Participants: 2,523 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 27,380 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 →