Elecsys plasma Aβ42 /Aβ40 could potentially rule out amyloid pathology in populations with low-to-moderate amyloid positivity prevalence. 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.
Evaluating potential therapies for Alzheimer's disease (AD) depends on use of biomarkers for appropriate subject selection and monitoring disease progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder characterised by progressive dementia, brain atrophy, and ultimately death. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The median Aβ1-42/1-40 ratio was 20.86% lower in amyloid-positive subjects than in the amyloid-negative group, while the median AβX-42/X-40 ratio was only 15.56% lower. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current diagnostic pathways are heterogeneous, meaning many AD patients are missed while low-risk patients undergo unnecessary procedures. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early and accurate diagnosis of Alzheimer's disease (AD) in clinical practice is urgent with advances in AD treatment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mild cognitive impairment (MCI) associated with physical frailty gave rise to the new concept of cognitive frailty. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In 2025, several major advances have marked the field of neurology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB), a synucleinopathy, is the second most common form of dementia after Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
BBBO was achieved in 5 out of 6 subjects with an average volume of 983±626 mm 3 following FUS at the right frontal lobe both in white and gray matter regions. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
There is little information on the dynamics of BDNF in the CSF in the continuum between healthy aging, MCI and AD. 2 key findings →
Participants: 128 Evidence: low
Full summary, score breakdown and related studies → Original source
CSF YKL-40 and chitotriosidase levels are increased in individuals with clinical FTD syndromes, particularly due to AD pathology. 4 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Rapamycin is not detectable in the CSF before or after treatment, but several Alzheimer's disease and inflammatory biomarkers increase after treatment. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
These results are comparable to previous reports using insulin resistance. 5 key findings →
Participants: 86 Evidence: low
Full summary, score breakdown and related studies → Original source
Shifts in the magnitude and nature of gut microbial metabolites have been implicated in Alzheimer's disease (AD), but the host receptors that sense and respond to these metabolites are largely unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
As novel, anti-amyloid therapies have become more widely available, access to timely and accurate diagnosis has become integral to ensuring optimal treatment of patients with early-stage Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Experimental data suggest that the cerebrospinal fluid (CSF) dynamic is involved in the clearance of beta-amyloid, a key event in the pathogenesis of Alzheimer's disease (AD). 4 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau181 levels were influenced by the presence of underlying AD pathology, independently from the cognitive status and were highly accurate in differentiating SCD-MCI patients who were carriers of AD pathology from non-carriers. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
To investigate potential associations between cerebrospinal fluid (CSF) microplastics and Alzheimer's disease (AD) pathology or cognitive function. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified numerous genetic variants associated with AD risk, while a transcriptomic analysis has revealed dysregulated gene expression patterns in the brains of individuals with AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma BD-tau and p-tau181 mimic their corresponding cerebrospinal fluid (CSF) markers. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma NfL and GFAP predict cognitive decline in a similar manner to traditional imaging techniques in amyloid-positive MCI patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Considering renal function and age is crucial when interpreting AD biomarkers in the general aging population. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An improved understanding of the pathobiology of Alzheimer's disease (AD) should lead ultimately to an earlier and more accurate diagnosis of AD, providing the opportunity to intervene earlier in the disease process and to improve outcomes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers for Alzheimer's disease (AD) are a promising tool that may help in early diagnosis. 2 key findings →
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 →