27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Models including plasma biomarkers yielded the most accurate predictions of tau-PET burden (best model: R-squared = 0.66-0.69), with especially high contribution from plasma phosphorylated tau-217 (p-tau217). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Phosphorylation renders the PRD significantly resistant to cleavage by the lysosome, especially at less acidic pH setpoints. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Elevated BMI/BV associated with lower BBM concentrations, especially for p-Tau217 and NfL, independent of brain amyloid burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Participants with SSD exhibited a greater increase in plasma NfL levels and more pronounced declines in global cognition, memory, executive function, language, and processing speed over 2 years compared to non-SSD participants. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
As the most prevalent form of dementia, Alzheimer's disease (AD) represents a major public health challenge. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers were associated with comorbidities and metabolites such as estimated glomerular filtration rate, homocysteine, and high-density lipoprotein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The maximum mean wait time under the current workflow was projected at 6.4 months, decreasing with BBM integration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As expected, males had higher lean mass and VO2peak than females (p = 0.01), but groups did not differ in body mass index (p = 0.51). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Participants rated the materials highly regarding value and comprehension. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to individuals carrying two copies of the ε4 allele of apolipoprotein E (APOE), ε2 homozygotes have an approximate 99% reduction in late-onset Alzheimer's disease (AD) risk. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sporadic Alzheimer's disease (sAD) is marked by dysregulated lipid metabolism, prominently involving apolipoprotein E (ApoE). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The APOE4 variant was the strongest genetic risk factor for sporadic Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE4-KI mice showed impaired retinal structure, vasculature, function, vision, increased gliosis and neuroinflammation, and downregulation of synaptogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia, a collective term for neurodegenerative disorders marked by cognitive decline, affects millions worldwide, and is expected to rise significantly in prevalence. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid/tau/neurodegeneration (ATN) biomarker framework has greatly progressed the diagnosis and staging of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ACAT1 inhibition increased LRP1 levels and soluble TREM2 (sTREM2) release via enhanced TREM2 cleavage by ADAM metallopeptidase domain 10/17 (ADAM10/17). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ms4a4a deficiency reduced steady-state Aβ levels and shortened its half-life in brain interstitial fluid. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In 5xFAD mice, the absence of PLCG2 resulted in reduced TREM2 expression and impaired microglial associations with amyloid beta plaques. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have identified many gene polymorphisms associated with an increased risk of developing late-onset Alzheimer's disease (LOAD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protective PLCG2P522R microglia showed significant transcriptomic similarity to isogenic controls. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Exercise's protective effects in Alzheimer's disease (AD) are well recognized, but cell-specific contributions to this phenomenon remain unclear. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Within each tracer, GMM-derived amyloid negative (A-) CL distributions were similar across cohorts. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
AD mice showed early decreases in NVC and bilateral connectivity (BC) in motor and cingulate cortex, and hypoconnectivity within the sensory-motor network. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As Alzheimer's disease (AD) research advances, tau has emerged as both a critical biomarker and a promising therapeutic target, central to understanding disease mechanisms, tracking progression, and guiding treatment development. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease, tau pathology spreads across brain regions as the disease progresses. 5 key findings →
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 →