28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
PDGFRβ levels were similar in CAA patients and controls (P = .78) and in aMCI/AD clinical phenotype and controls (P = .91). aMCI/AD patients with an AD+ biomarker profile (A+T+[N+]) had increased PDGFRβ levels compared to (A-T-[N-]) controls (P = .006). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In women we found a significant correlation between CSF amyloid-beta (Aβ1-42) and several subtests measuring delayed recall. 3 key findings →
Participants: 79 Evidence: low
Full summary, score breakdown and related studies → Original source
We explored the relationship between cerebrospinal fluid (CSF) tau levels as indirect markers of tau-related pathology in Alzheimer's disease (AD) and EEG slowing, a typical neurophysiological finding in the disease. 1 key finding →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
For all patients across both groups, an association between PGRN and categoric (p = 0.016) and letter fluency (p = 0.029), naming (p = 0.003), and overall cognition (Mini-Mental State Examination: p = 0.04) was observed. 5 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source
Earlier studies have shown elevated levels of tau protein and decreased levels of amyloid beta42 in cerebrospinal fluid (CSF) from patients with Alzheimer's disease (AD). 3 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
The Abeta(1-42), T-tau and P-tau(181) levels in PCA patients differed significantly (p < 0.02) from those in healthy controls but were indistinguishable from subjects with a clinical diagnosis of AD. 3 key findings →
Participants: 34 Evidence: low
Full summary, score breakdown and related studies → Original source
The APOE-npscore explained more variance and provided a better model fit for all three CSF measures than APOE ε4-carrier status and ε4 allele count. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The main objective was to investigate the acetylcholinesterase E (AChE) activity in the cerebrospinal fluid (CSF) of patients with three common dementia disorders. 3 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular factors are thought to contribute to the development of disease pathology in neurodegenerative dementia such as Alzheimer's disease (AD). 1 key finding →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
Potential cerebrospinal fluid (CSF) markers for Alzheimer's disease (AD) include tau protein, the 42 amino-acid form of amyloid beta (amyloid beta(1-42)) and apolipoprotein E (apoE). 2 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source
The two most frequently examined biomarkers in the diagnosis of dementia are cerebrospinal fluid (CSF) tau and beta-amyloid(1-42) (Abeta(1-42)). 4 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
The (pre-)analytical procedures were similar between centers. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
p-Tau181 levels were higher in the lvPPA-AD group than in the aMCI-AD group (p < 0.05). 3 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
Tau protein concentrations were measured in the CSF of 23 patients with dementia of the Alzheimer type (DAT), 36 patients with multi-infarct dementia (MID), and 23 control subjects. 2 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
Being treatable, steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), or Hashimoto's encephalopathy, should be distinguished from untreatable conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the MCI group, age (B = -0.37, p<0.001) and current daily use of computer-based devices (B = 5.85, p<0.001) were associated with the number of correct cancellations of the e-CT. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sixteen semi-structured interviews were conducted with nine participants, at two-time points. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For the reproducibility, identical P-values and slope estimates were found with both digital biomarkers and neuropsychological test measures between the previous and current studies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early cognitive changes due to Alzheimer's disease (AD) include difficulties in semantic access and working memory. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Health-monitoring technologies for automatically detecting the early signs of Alzheimer's disease (AD) have become increasingly important. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The mean DDAF score was 40.56 ± 21.18 among digital natives (18-29 years), 34.93 ± 21.88 among the digital transition generation (30-44 years), and 25.17 ± 18.59 among digital immigrants (45-70 years) (p < 0.001). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (ApoE) mediates the bidirectional transport of lipids between cells. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that TDP-43 overexpression induced motor function deficits, neuronal loss, and gliosis in the motor cortex, especially in APOE2 mice, with much milder or absent effects in APOE3, APOE4, or Apoe-KO mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE4 is a strong genetic risk factor for Alzheimer's disease and Dementia with Lewy bodies; however, how its expression impacts pathogenic pathways in a human-relevant system is not clear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Liver-generated plasma apolipoprotein E (apoE) does not enter the brain but nonetheless correlates with Alzheimer's disease (AD) risk and AD biomarker levels. 4 key findings →
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 →