A total of 73% of patients had a low coenzyme Q10 status. 5 key findings →
Participants: 73 Evidence: low
Full summary, score breakdown and related studies → Original source
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
A total of 73% of patients had a low coenzyme Q10 status. 5 key findings →
Participants: 73 Evidence: low
Full summary, score breakdown and related studies → Original source
The levels of four CSF biomarkers correlated to EOAD signature atrophy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative and inflammatory processes influence the clinical course of multiple sclerosis (MS). 1 key finding →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
The assay had a reportable range of 100 to 25000 pg/mL, a limit of quantification of 100 pg/mL, recoveries between 93% and 111%, and intraassay and interassay CV <15% for both peptides. 4 key findings →
Participants: 102 Evidence: low
Full summary, score breakdown and related studies → Original source
Nine PSEN2 rare variants were found, including two reported (M239T, R62C) and seven novel variants (N141S, I368F, L396I, G117X, I146T, S147N, H220Y). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We sought to identify a usable biomarker from blood samples to characterize early-stage Alzheimer's disease (AD) patients, in order to facilitate rapid diagnosis, early therapeutic intervention, and monitoring of clinical trials. 1 key finding →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source
The proteomic profile discriminated DLB and PD from NC with an AUC (Area Under the Curve) of 0.96 with demographics of age, sex and education. 4 key findings →
Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source
The novel IP-MS assay measuring the Aβ42/40 ratio demonstrated an AUC of 0.82 for differentiating AD from control subjects. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau181 level showed certain discrepancies between NC and MCI (p < 0.05), AD (p < 0.01) groups. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found brain volume reduction in the bilateral temporal, amygdala, parahippocampal and lower parietal lobe and left cingulate and precuneus regions (family-wise error, p < 0.05). 4 key findings →
Participants: 162 Evidence: low
Full summary, score breakdown and related studies → Original source
There were significant positive correlations between the predicted MMSE scores and ground truth scores in the Patient and Healthy groups (r = 0.66, p < 0.001). 5 key findings →
Participants: 202 Evidence: low
Full summary, score breakdown and related studies → Original source
Among participants enrolled, the median (interquartile range) age was 57 (28.5-75) years and 5.8% had AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with idiopathic normal pressure hydrocephalus (iNPH) frequently show pathologic CSF Aβ42 levels, comparable with Alzheimer's Disease (AD). 5 key findings →
Participants: 44 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) amyloid-β (Aβ)42 and tau are biomarkers for Alzheimer's disease (AD); however, the effects of other neurodegenerative processes on these biomarkers remain unclear. 2 key findings →
Participants: 213 Evidence: low
Full summary, score breakdown and related studies → Original source
Postmortem brain studies of older drivers killed in car accidents indicate that many had Alzheimer disease (AD) neuropathologic changes. 2 key findings →
Participants: 129 Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction is the best anatomical correlate of early cognitive impairment in Alzheimer's disease (AD). 4 key findings →
Participants: 210 Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunctions precede cognitive decline in Alzheimer's disease by decades, affect executive functions, and can be detected by quantitative electroencephalography (qEEG). 4 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Different clinical variants of probable Alzheimer's disease (AD) share underlying plaques and tangles but show distinct atrophy patterns. 2 key findings →
Participants: 52 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is a small vessel disease characterized by the deposition of amyloid-beta in small cerebral vessels, which can lead to intracerebral hemorrhages and cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the total sample, T-tau and Aβ42/p-tau correlated with the total CAMCOG (P < .01); all biomarkers correlated with memory (P < .001); T-tau correlated with language (P < .01). 3 key findings →
Participants: 51 Evidence: low
Full summary, score breakdown and related studies → Original source
MCI-AD patients yielded larger P50s than MCI-Other. 4 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
After correction for age, sex, and education, CSF tau levels were found to be negatively related to the Visual Association Test (standardized β = -0.3, P < .05), whereas CSF Aβ1-42 levels were found to be positively related to the Mini-Mental State Examination (β = 0.3, P < .05), the frontal assessment battery (β = 0.5, P < .05), and digit span backwards test (β = 0.3, P = .01). 5 key findings →
Participants: 58 Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to cognitively normal subjects, AD-spectrum patients (i.e., EMCI, LMCI, and AD) showed a reversing trend toward an association between CSF pathological markers and the abnormal SRN occurring during the progression of AD. 3 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Co-existence of Alzheimer's disease (AD) in normal pressure hydrocephalus (NPH) is a frequent finding, thus a common pathophysiological basis between AD and NPH has been postulated. 2 key findings →
Participants: 294 Evidence: low
Full summary, score breakdown and related studies → Original source
The need for effective treatments halting Alzheimer's disease (AD) urges the discovery of the earliest possible biomarkers. 3 key findings →
Participants: 20 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →