Tau-mediated neurodegeneration is a hallmark of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tau-mediated neurodegeneration is a hallmark of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The plasma p-tau217 and plasma GFAP models adequately predicted the change over time, with donanemab resulting in decreased plasma p-tau217 and plasma GFAP concentrations. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease(AD) is being the burden of society and family. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Patients were followed for a median of 2.92 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Evaluating potential therapies for Alzheimer's disease (AD) depends on use of biomarkers for appropriate subject selection and monitoring disease progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current diagnostic pathways are heterogeneous, meaning many AD patients are missed while low-risk patients undergo unnecessary procedures. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early and accurate diagnosis of Alzheimer's disease (AD) in clinical practice is urgent with advances in AD treatment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The APOE-npscore explained more variance and provided a better model fit for all three CSF measures than APOE ε4-carrier status and ε4 allele count. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early cognitive changes due to Alzheimer's disease (AD) include difficulties in semantic access and working memory. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found that TDP-43 overexpression induced motor function deficits, neuronal loss, and gliosis in the motor cortex, especially in APOE2 mice, with much milder or absent effects in APOE3, APOE4, or Apoe-KO mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Seventeen variants were significantly associated with AD within five genomic regions implicating the genes OARD1/NFYA/TREML1, JAZF1, FERMT2, and SLC24A4. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex genetic disease, and variants identified through genome-wide association studies (GWAS) explain only part of its heritability. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
During the 4-day meeting, presenters illuminated aspects of the cross-talk between APOE and immunity, with a focus on the roles of microglia, triggering receptor expressed on myeloid cells 2 (TREM2), and components of inflammation (e.g., tumor necrosis factor α [TNFα]). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common neurodegenerative disease, characterized by dementia and premature death. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Due to commonalities in pathophysiology, age-related macular degeneration (AMD) represents a uniquely accessible model to investigate therapies for neurodegenerative diseases, leading us to examine whether pathways of disease progression are shared across neurodegenerative conditions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A repeat expansion in the C9orf72 (C9) gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Retromer controls cellular homeostasis through regulating integral membrane protein sorting and transport and by controlling maturation of the endo-lysosomal network. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Most participants were cognitively normal (427 of 491 [87%]) and the mean age was 69.0 ± 8.8 years. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It remains unclear why β-amyloid (Aβ) plaque, a hallmark pathology of Alzheimer's disease (AD), first accumulates cortically in the default mode network (DMN), years before AD diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, the U.S. Food and Drug Administration (FDA) approved 2 anti-amyloid monoclonal antibodies, aducanumab (June 7, 2021) and lecanemab (July 6, 2023), for the treatment of Alzheimer's disease (AD) patients, and will most likely also approve a 3rd one, donanemab, soon. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hardy and Mummery discuss the recent positive findings in the clinical trial of lecanemab in early Alzheimer’s disease, and the implications for the amyloid hypothesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Out of 538 articles, 23 (4.27%) were published in journals from the geriatric category, 44 (8.18%) included an author affiliated with a geriatric institution. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study focused on designing and evaluating Tau-PET tracers for noninvasive positron emission computed tomography (PET) imaging of neurofibrillary tangles (NFTs), a hallmark pathology of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Crude AD prevalence (2015-2020) was estimated at 760.5 per 100,000 inhabitants, and age-standardized prevalence (2020) was 664.6 (male 595.7, female 711.0). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
GBA-related PD (GBA-PD) patients have higher risk of dementia and reduced survival than non-carriers. 3 key findings →
Design: open-label trial Evidence: low
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 →