28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
β-blockers that easily cross the blood-brain barrier (BBB) seem to diminish the risk of Alzheimer's disease (AD), hypothetically facilitating waste clearance. 3 key findings →
Participants: 216 Evidence: low
Full summary, score breakdown and related studies → Original source
We assessed cerebrospinal fluid (CSF) levels of tau and other biomarkers of neurodegenerative disease. 4 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Numerous imaging variables differed by clinical diagnosis, including hippocampal, amygdalar and inferior lateral ventricular volumes and entorhinal, lingual, inferior parietal and isthmus cingulate cortical thicknesses, at a false discovery rate (FDR)-corrected threshold for significance (analysis of covariance; p < 0.005). 3 key findings →
Participants: 191 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration, the neuropathological substrate of frontotemporal dementia (FTD), is characterized by the deposition of protein aggregates, including tau. 4 key findings →
Participants: 99 Evidence: low
Full summary, score breakdown and related studies → Original source
In HC and MCI subjects, FBP PET anterior and posterior cingulate and composite standard uptake value ratios correlated with CSF amyloid beta (Aβ1-42) and tau/Aβ1-42 ratios. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
Plasma pTau217 and pTau181 both correlate with AD, but the fold change in pTau217 makes it better to diagnose cerebral amyloidosis, and predict cognitive decline and conversion to AD dementia. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Clinical trials testing tau-targeting therapies may benefit from using fluid biomarkers to recruit individuals at risk of tau aggregation. 1 key finding →
Participants: 163 Evidence: low
Full summary, score breakdown and related studies → Original source
The association between reduced CSF α-synuclein concentrations and cognition suggests that α-synuclein pathology contributes to early cognitive impairment in PD, in particular to executive-attentional dysfunction. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
These results support plasma p-tau 181 for the detection of AD dementia and the use of blood-based biomarkers for optimal disease detection. 2 key findings →
Participants: 235 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers of dementia, including phosphorylated tau (p-tau217), offer promise as tools for diagnosis, stratification for clinical trials, monitoring disease progression, and assessing the success of interventions in those living with Alzheimer's disease. 2 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
[ 18 F]PSS232 PET can quantify the changes of mGluR5 availability in the progression of AD. mGluR5 availability correlated not only with neuropathological biomarkers of AD but also with neurodegenerative biomarkers and cognitive performance. mGluR5 may be a novel neurodegenerative biomarker, and whether mGluR5 could be a potential therapeutic target for AD needs to be further studied. 4 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source
To investigate the association between serum neurofilament light chain (NfL) levels, inflammatory cytokines, and cognitive function to assess their utility in the early detection of mild cognitive impairment (MCI). 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 3,322 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →