High CSF p-tau and low ratios of Aβ(1-42)/Aβ(1-40) and Aβ(1-42)/Aβ(1-38), respectively, were specific for AD. 5 key findings →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,780 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
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 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
45/100
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
45/100
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
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
We identify novel genome-wide significant associations between DNA variants in TMEM106B and CSF levels of NfL, and between CPOX and YKL-40. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Most participants were cognitively normal (427 of 491 [87%]) and the mean age was 69.0 ± 8.8 years. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
With the recent approval by the FDA of the first disease-modifying drug for Alzheimer's Disease (AD), personalized medicine will be increasingly important for appropriate management and counseling of patients with AD and those at risk. 1 key finding →
Evidence: moderate
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
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
From across this tag
10 of the 3,069 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Mild cognitive impairment due to cerebrovascular disease and Alzheimer’s
- Molecular neuropsychology: creation of test-specific blood biomarker algorithms
- GFAP and vimentin deficiency alters gene expression in astrocytes and microglia in wild‐type mice and changes the transcriptional response of reactive glia in mouse model for A lzheimer's disease
- Concordance between brain 18F-FDG PET and cerebrospinal fluid biomarkers in diagnosing Alzheimer's disease
- Plasma p-Tau217 and GFAP predict widespread cognitive decline in Alzheimer's disease
- Mass spectrometry-based methods for robust measurement of Alzheimer's disease biomarkers in biological fluids
- Association of [ 18 F]Flortaucipir–PET and Plasma p-Tau217 With Tau Neuropathology in Alzheimer Disease and Other Neurodegenerative Disorders
- From Cerebrospinal Fluid to Blood: The Third Wave of Fluid Biomarkers for Alzheimer's Disease
- Cerebrospinal Fluid Markers of Synaptic Injury and Functional Connectivity in Alzheimer Disease: Protocol for a Cross-Sectional Study
- Association of Cerebrospinal Fluid Neurofilament Light Concentration With Alzheimer Disease Progression
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →