Phosphorylated-tau 217 (pTau217) is currently the most promising blood-based biomarker for accurately detecting Alzheimer's disease (AD) pathology. 3 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.
Alzheimer's disease (AD) presents a critical global challenge, accounting for over 60 % of the 57 million current dementia cases worldwide, with prevalence projected to exceed 100 million by 2050. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Validated plasma phosphorylated tau 217 (p-tau217) assays identify Alzheimer disease pathology with high accuracy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) measures of phosphorylated-tau (P-tau) 231 and P-tau181 are two biomarkers for the identification of tau pathology as related to Alzheimer's disease (AD). 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
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
We observed a significant CSF Aβ42 /Aβ40 × p-tau interaction on cortical neurite density index (NDI), but not orientation dispersion index or cortical thickness. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
After correction for multiple comparisons, a strong positive association between CSF Abeta42 levels and glucose metabolism was identified for 2 extensive clusters located in the right temporal, prefrontal and anterior cingulate cortices. 3 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
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
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 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
Alzheimer's disease (AD) is the most common cause of dementia in older people. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
8 of the 707 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 8. The same 8 appear here every time.
- Analytical performance of a delayed-centrifugation blood collection tube for remote blood biomarker assessment
- Plasma phosphorylated-tau181 as a predictive biomarker for Alzheimer's amyloid, tau and FDG PET status
- Targeted Mass Spectrometry Suggests Beta-Synuclein as Synaptic Blood Marker in Alzheimer's Disease
- Cerebrospinal fluid α-synuclein predicts neurodegeneration and clinical progression in non-demented elders
- The potential clinical value of plasma biomarkers in Alzheimer's disease
- Amyloid and Tau Cerebrospinal Fluid Biomarker Normalization in a Patient with Alzheimer’s Disease treated with Lecanemab: A Case Report
- Proteomic studies of cerebrospinal fluid biomarkers of Alzheimer's disease: an update
- Genetic risk and plasma biomarkers of dementia with Lewy bodies in a Chinese population
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 →