28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Recently, cerebrospinal fluid (CSF) YKL-40 levels were reported to be a promising candidate biomarker of glial inflammation in Alzheimer's disease (AD). 2 key findings →
Design: cross-sectional Participants: 63 Evidence: low
Full summary, score breakdown and related studies → Original source
We aimed to evaluate the specificity of neurogranin (Ng) for Alzheimer's disease (AD) in a dementia cohort. 2 key findings →
Participants: 116 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid positron emission tomography (PET) and cerebrospinal fluid (CSF) amyloid beta (Aβ)42/phosphorylated tau (p-tau)181 showed excellent performance in differentiating autopsy-confirmed AD and predicting the risk of neuropathological changes in early and late clinical stages. 5 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
We found statistically significant batch differences for all biomarkers and ratios, except that neurofilament light was comparable between batches 1 and 2. 4 key findings →
Participants: 528 Evidence: low
Full summary, score breakdown and related studies → Original source
Voxel-based analyses demonstrated significant negative correlations between CSF tau and ptau(181) levels and CMRglu in the posterior cingulate, precuneus, and parahippocampal regions. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Comparing the discordant CSF results of each patient with the cerebral amyloid-PET results, we found that in the group with Aβ1 - 42+ and p-tau-CSF values, the amyloid-PET was positive in 51.2% and negative in 48.8% of patients, while in the group with Aβ1 - 42-and p-Tau+ CSF values, the amyloid-PET was positive in 52.6% of patients and negative in 47.4% of them. 4 key findings →
Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source
Studies have shown that multimorbidity may be associated with the Alzheimer's disease (AD) stages, but it has not been fully characterized in patients without dementia. 5 key findings →
Participants: 1,402 Evidence: low
Full summary, score breakdown and related studies → Original source
BackgroundCognitive impairment significantly impacts the quality of life in patients with neurodegenerative disorders, including Huntington's disease (HD), Parkinson's disease (PD), and Alzheimer's disease (AD).ObjectiveThis study aims to assess the utility of MemTrax, a contemporary digital continuous recognition task platform originally developed for AD, as an effective tool for revealing cognitive and clinical motor impairments in HD and PD populations as aligned with respective disease staging. 2 key findings →
Participants: 135 Evidence: low
Full summary, score breakdown and related studies → Original source
In response to correspondence from Cognivue, Inc. regarding our publication (Jannati et al., 2025), we clarify that our analysis employed a rigorous paired-sample design using the same 930 participants from the Bio-Hermes-001 study for both the Digital Clock and Recall® (DCR) and Cognivue Clarity® assessments. 3 key findings →
Participants: 930 Evidence: low
Full summary, score breakdown and related studies → Original source
Baseline data predicted that 36 patients with MCI would progress to the AD clinical syndrome (ADS Progressing). 4 key findings →
Participants: 107 Evidence: low
Full summary, score breakdown and related studies → Original source
A high Pearson correlation coefficient of 0.77 (CI = 0.63-0.86) was observed between the two scores. 5 key findings →
Participants: 55 Evidence: low
Full summary, score breakdown and related studies → Original source
Disrupted iron homeostasis is associated with several neurodegenerative diseases, including Alzheimer's disease (AD), and may be partially modulated by genetic risk factors. 4 key findings →
Participants: 27,535 Evidence: low
Full summary, score breakdown and related studies → Original source
Niemann-Pick disease, type C1 (NPC1) is a lipid storage disorder that results in progressive neurological impairment. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mutation screening revealed a novel probably pathogenic mutation (PSEN1 p.Leu232Phe). 3 key findings →
Participants: 450 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers offer strong potential to revolutionize diagnosis, trial enrolment and treatment monitoring in Alzheimer's disease (AD). 3 key findings →
Participants: 962 Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this paper is to systematically evaluate a biased sampling issue associated with genome-wide association analysis (GWAS) of imaging phenotypes for most imaging genetic studies, including the Alzheimer's Disease Neuroimaging Initiative (ADNI). 3 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We obtained a predictive accuracy of 0.71 (95 % CI [0.59, 0.84]) with an AUC of 0.69 in the HRS test dataset and got an accuracy of 0.62 (95 % CI [0.56, 0.68]) with an AUC of 0.63 in the ROSMAP dataset. 3 key findings →
Participants: 234 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Levels of sociability are continuously distributed in the general population, and decreased sociability represents an early manifestation of several brain disorders. 5 key findings →
Participants: 342,461 Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated which factors might explain the differences between the frequencies of brain β-amyloid (Aβ) deposition in Korean and European cognitively normal individuals (CNs). 1 key finding →
Participants: 434 Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies have reported that a rare nonsynonymous variant rs75932628-T in the TREM2 gene is associated with increased risk of Alzheimer's disease and Parkinson's disease (PD) in European-descended populations. 2 key findings →
Participants: 908 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified 133 unique and shared metabolites associated with ADAD, TREM2, and sAD. 5 key findings →
Participants: 133 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrovascular dysregulation is a hallmark of Alzheimer's disease (AD), but the changes that occur in specific cell types have not been fully characterized. 1 key finding →
Participants: 220 Evidence: low
Full summary, score breakdown and related studies → Original source
Survivors of childhood cancer are prone to neurocognitive impairment and premature aging, raising concerns about early onset dementia. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Fusion of all five data modalities (n = 111) yielded two subtypes (n S1 = 53, n S2 = 58), which were nominally associated with diffuse amyloid plaques; however, this effect was not significant after correction for multiple testing. 5 key findings →
Participants: 111 Evidence: low
Full summary, score breakdown and related studies → Original source
Apraxia of speech is a motor speech disorder characterized by combinations of slow speaking rate, abnormal prosody, distorted sound substitutions, and trial-and-error articulatory movements. 1 key finding →
Design: cross-sectional Participants: 14 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 →