27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In regression analyses across the whole study sample adjusted for age, sex, and diagnostic group, there was no relationship between HbA1c or fasting glucose and CSF tau, p-tau 182, or Abeta42 levels. 3 key findings →
Design: cross-sectional Participants: 91 Evidence: low
Full summary, score breakdown and related studies → Original source
At genera and species levels, higher subgingival periodontal dysbiosis was associated with reduced CSF amyloid beta (Aβ)42 (P = 0.02 and 0.01) but not with P-tau. 3 key findings →
Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source
We included 201 individuals (mean age 73.5 years, mean BMI 27.4 kg/m2). 4 key findings →
Participants: 201 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 96 proteins were decreased in MCI-SNAP compared to CN and MCI-AD. 5 key findings →
Participants: 96 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral microbleeds (CMBs) are hypothesised to have an important yet unknown role in the dementia disease pathology. 4 key findings →
Participants: 1,039 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Thirteen pathway clusters were identified, and eight pathway-specific PRSs were significantly associated with AD diagnosis. 5 key findings →
Participants: 1,411 Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenic relevance in Alzheimer's disease (AD) presents a decrease of cerebrospinal fluid amyloid-ß42 (Aß42) burden and an increase in cerebrospinal fluid total tau (T-tau) levels. 3 key findings →
Participants: 843 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Using the data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), we performed a genome-wide association study (GWAS) between 565,373 single nucleotide polymorphisms (SNPs) and 16 key AD biomarkers from 1,576 subjects at four visits. 5 key findings →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
Accurate staging of Alzheimer's disease (AD) pathology is crucial for therapeutic trials and prognosis, but existing fluid biomarkers lack specificity, especially for assessing tau deposition severity, in amyloid-beta (Aβ)-positive patients. 2 key findings →
Participants: 136 Evidence: low
Full summary, score breakdown and related studies → Original source
Based on retrospective data, we develop personalized risk estimates for MCI patients. 4 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
All Centiloid cut-offs fell within the range of 25-35, except for CSF Aβ42 that rendered an optimal cut-off value of 12 CL. 5 key findings →
Participants: 205 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found a significant correlation of CSF α-syn level with PM2.5 in urban participants. 4 key findings →
Participants: 933 Evidence: low
Full summary, score breakdown and related studies → Original source
P‐tau181 in CSF and plasma predicted tau accumulation (r > 0.36, P < .001), even in AD‐continuum individuals with normal baseline tau‐PET (A+T–; r > 0.37, P < .05). 4 key findings →
Participants: 163 Evidence: low
Full summary, score breakdown and related studies → Original source
Infections have been associated with the incidence of Alzheimer disease and related dementias, but the mechanisms responsible for these associations remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We established AD diagnostic models using plasma biomarkers for Chinese participants. 2 key findings →
Participants: 159 Evidence: low
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Participants with higher total-tau and NfL at baseline had a higher risk of stroke and several stroke subtypes. 5 key findings →
Participants: 379 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results support the utility of CSF VEC as a marker of endothelial injury in AD and highlight the importance of endothelial injury as an early pathology that contributes to cognitive impairment in even the earliest preclinical stages. 3 key findings →
Participants: 700 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Twenty-seven individuals (14%) had an abnormal amyloid PET, and 14 twin-pairs (15%) showed discordant amyloid PET scans. 2 key findings →
Participants: 126 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Comparing clinical stages, CSF PDGFRβ levels were increased at the MCI stage (Cohen's d = 0.55 [CI 95% 0.066, 1.0], P = 0.025) compared with NC. 3 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that microglial and astrocyte reactivity, measured through fluid biomarkers, occur early and impact the amyloid cascade on the preclinical Alzheimer´s continuum. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Magnetic resonance spectroscopy detects Alzheimer's disease related inflammation and neurodegeneration, and could be a good noninvasive disease-stage biomarker in Down syndrome. 3 key findings →
Participants: 118 Evidence: moderate
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There is growing evidence that cognitive decline can be affected by both nutritional aspects and inflammation. 3 key findings →
Design: cross-sectional Participants: 116 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Determining blood biomarkers represents less invasive and less costly diagnostics for Alzheimer´s disease. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Clusters of CSF biomarker levels are related to cognitive profiles in Alzheimer disease. 1 key finding →
Participants: 177 Evidence: low
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CSF Abeta1-14, Abeta1-15, and Abeta1-16 increase during gamma-secretase inhibitor treatment in AD, even at doses that do not affect Abeta1-42 or Abeta1-40, probably because of increased substrate availability of the C99 APP stub (APP beta-CTF) induced by gamma-secretase inhibition. 2 key findings →
Participants: 35 Evidence: high
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 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 →