46/100
Eighty (22%) participants were APOE ε4 carriers and 290 (73%) were non-carriers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid β (Aβ) peptides are important components of plaques in patients with Alzheimer's disease (AD). 1 key finding →
Participants: 370 Evidence: low
Full summary, score breakdown and related studies → Original source
Both cohorts revealed diminished choriocapillaris signals, demonstrating the highest discriminatory capability (area under the receiver operating characteristic curve: SS-OCTA 0.913, SD-OCTA 0.991; P < 0.001). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the population ages, neurodegenerative diseases are becoming more prevalent, making it crucial to comprehend the underlying disease mechanisms and identify biomarkers to allow for early diagnosis and effective screening for clinical trials. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The life expectancy of people with multiple sclerosis (MS) has increased, yet we have noted that development of a typical Alzheimer disease dementia syndrome is uncommon. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The maximum mean wait time under the current workflow was projected at 6.4 months, decreasing with BBM integration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As expected, males had higher lean mass and VO2peak than females (p = 0.01), but groups did not differ in body mass index (p = 0.51). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Specific biomarkers in a readily accessible biological fluid, such as blood, could aid in the identification, characterization, validation, and routine monitoring of Alzheimer's disease (AD) progression. 5 key findings →
Participants: 135 Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
GFAP did not correlate with Aβ- or tau-PET cross-sectionally. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
Synaptic degeneration is a major hallmark of Alzheimer's disease (AD) and the best pathological correlate of cognitive dysfunction. 3 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Participants rated the materials highly regarding value and comprehension. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
CKD patients showed elevated levels of neurofilament light (117 ± 72 vs. 11 ± 5 pg/mL), phosphorylated tau 181 (75 ± 42 vs. 13 ± 8 pg/mL), glial fibrillary acidic protein (193 ± 127 vs. 94 ± 39 pg/mL), amyloid β 42 (17 ± 5 vs. 5 ± 1 pg/mL), and amyloid β 40 (259 ± 96 vs. 72 ± 17 pg/mL) compared to controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The 88 patients with AD included 15 with microbleeds only in cortical/subcortical regions (cortical microbleeds) that could be CAA-related, 16 with microbleeds only in deep locations (deep microbleeds), 3 with microbleeds in both cortical and deep locations (mixed microbleeds), and 54 without microbleeds. 4 key findings →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
CSF AβR better agreed with Amy-PET compared to CSF Aβ42 (Cohen's K 0.431 versus 0.05). 3 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source
Only a few individuals were A+T+Ng-. A+T+Ng+ and A+T+NfL+ showed different proteomic profiles compared to A+T+Ng- and A+T+NfL-, respectively. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we sought for a cerebrospinal fluid (CSF) metabolomic fingerprint in Alzheimer's disease (AD) patients characterized, according to the clinical picture and CSF AD core biomarkers (Aβ42, p-tau, and t-tau), both at pre-dementia (mild cognitive impairment due to AD, MCI-AD) and dementia stages (ADdem) and in a group of patients with a normal CSF biomarker profile (non-AD) using untargeted 1H nuclear magnetic resonance (NMR) spectroscopy-based metabolomics. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found a significant increase in the concentrations of ZnT3, GluA3, and Dynamin1 in AD (p = 0.002) and of ZnT3 and Dynamin 1 in DLB (p = 0.001, p = 0.002) when compared to SCD patients. 4 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
Lower levels of NFL, NG, Aβ42, and t-tau were found in patients with iNPH versus SIVD, while YKL-40 and p-tau were similar in the two diseases. 4 key findings →
Participants: 28 Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
CSF-sLR11 concentrations were higher in patients with AD than controls (adjusted for sLR11 using phospholipid). 3 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) biomarkers have been extensively investigated in idiopathic normal pressure hydrocephalus (iNPH) with the aim of a better differential diagnosis, but the pathophysiological mechanisms underlying CSF biomarker changes and the relationship between biomarker levels and clinical variables are still a matter of debate. 3 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) neurofilament light (NFL) is a protein biomarker of axonal injury. 2 key findings →
Participants: 77 Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
The ratio CSF p-tau/t-tau was significantly higher in the NC group than that in the AD or OD groups (P<0.0005 for each group). 5 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
Plasma tau was negatively correlated with GMD in the medial temporal lobe (MTL), precuneus, thalamus, and striatum. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Mild cognitive impairment (MCI) often precedes Alzheimer's Dementia (AD), and in a high proportion of individuals affected by MCI, there are already neuropathological processes ongoing that become more evident when patients progress to AD. 3 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
As compared to the non-SSD group, the SSD group displayed lower CSF Aβ1-42 levels (β = -24.293, S.E. = 6.345, P < 0.001). 5 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →