28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
To gain insight of the underlying mechanisms of astroglial response to Alzheimer's disease (AD), the level of glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) from controls and AD subjects were immunochemically determined, and the correlation between that level and dementia severity of AD patients was evaluated. 3 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes are one of the brain's major cell types and are responsible for maintaining neuronal homeostasis via regulating the extracellular environment, providing metabolic support, and modulating synaptic activity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Altered concentrations of two out of three MMPs investigated in this study suggest that this family of biomolecules may play a role in the AD pathophysiology. 3 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
There is an association between plasma GFAP and regional 18F-SMBT-1 PET, and this association appears to be dependent on brain Aβ load. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest that VILIP-1 may play a role in the AD pathophysiology and is a good candidate for dynamic biomarker of AD, although this issue requires further investigation. 3 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
Depressed individuals are twice as likely to develop Alzheimer's disease (AD) as compared to controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ) fibrils in neuritic plaques are a hallmark of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gait disturbances are some of the earliest changes in dementia and their monitoring presents an opportunity for early diagnosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma amyloid β-42 (Aβ42) and Aβ42/Aβ40 are increasingly recognized as biomarkers for dementia, with low levels indicating increased risk. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
CD22 has been suggested to contribute to Alzheimer's disease (AD) pathogenesis by inhibiting microglial amyloid β (Aβ) phagocytosis. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
KRG administration showed the Lactobacillus dominance in the gut microbiota. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of cognitive decline worldwide, occurring in about 10% of people older than 65 years. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Treatment with the ABCA1 agonist CS-6253 appears to favor Aβ clearance from the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The results, specifically that lower serum IGF-I was associated with cognitive impairment, suggest that metabolism of IGF-I may be involved in the pathogenesis of cognitive deficits in Alzheimer's disease. 4 key findings →
Participants: 81 Evidence: low
Full summary, score breakdown and related studies → Original source
Several iPSC-derived three-dimensional (3D) cultures have been generated to model Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Serum NGAL levels are increased in DS and associated with distinct species of Aβ depending on the progression of dementia as diagnosed by baseline and follow-up clinical assessments. 5 key findings →
Participants: 67 Evidence: low
Full summary, score breakdown and related studies → Original source
Expression of iAβ42 in healthy Wistar rats predominates in the same structures where iAβ accumulates and Aβ plaques initially form in the much used, Wistar based McGill-R-Thy1-APP rat model for AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pathogenesis of presymptomatic disease stages remains elusive, although studies suggest that the early structural and functional alterations likely occur at neuronal dendritic spines. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical case study and functional characterization of the disease-associated presenilin-1 (PSEN1) mutations may help reveal the roles of PSEN1 in the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The novel PSEN1 M139L mutation found in familial AD increases the Aβ42/Aβ40 ratio significantly. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Serum C5a level increased with AD severity, and its expression was positively correlated with serum pro-inflammatory factor levels, and negatively correlated with cognitive function. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
BCG vaccine has been used for 100 years to prevent tuberculosis. 3 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
The K311R mutation might contribute to AD pathogenesis by overproducing toxic Aβ species and enhancing tau phosphorylation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex multifactorial disorder that poses a substantial burden on patients, caregivers, and society. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified the feasibility of a blood-based biomarker approach in AD diagnostics though the results warrant validation in large-scale studies. 3 key findings →
Participants: 90 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →