Onset-predictive biomarker tests (OPBTs) for genetic frontotemporal dementia (FTD) may predict symptom onset in coming years. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Concentrations of CSF APP were significantly lower in T- compared to T+ individuals across all clinical diagnostic groups across cohorts, regardless of A± status (Figure 1). 5 key findings →
Participants: 384 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We observed two promising biomarkers of AD, mLOY and APR, both contribute discriminating AD and CI but differently. 5 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
For the 30 clinically-diagnosed DLB participants, 23 (77%) were SAA-positive. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Biomarkers specific to AD pathology (p-tau217, GFAP) rather than peripheral inflammation had robust prognostic value in established AD. 5 key findings →
Participants: 333 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Integrating EEG features with plasma biomarkers improves prediction of cognitive function from mild cognitive impairment to moderate dementia, pending external validation. 1 key finding →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Aβ 42 , TDP-43, and neurogranin show potential as blood-based biomarkers for cognitive decline and may provide insight into the pathogenesis of neurodegeneration. 3 key findings →
Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
and neurogranin changes correlated with sabirnetug-AβO target engagement (p ≤ 0.01). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Twenty-nine individuals were enrolled, 3 were women (10.3 %), age 76.3 ± 6 years (mean ± SD). 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The number of patients with Alzheimer's Disease (AD) and other types of dementia disorders has drastically increased over the last decades. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Previous studies on blood-based biomarkers for Alzheimer's disease suggest a less invasive blood test might be a valuable screening tool for Alzheimer-specific pathology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ever since the discovery of APOEɛ4 around 25 years ago, researchers have been excited about the potential of a blood test for Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To elucidate an involvement of amyloid dysmetabolism in the pathophysiology of depression, we investigated associations of plasma amyloid-β (Aβ) levels with Alzheimer's disease-related changes in neuroimaging and cognitive dysfunction in patients with late-life depression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Alzheimer's disease (AD)-a complex disease showing multiple pathomechanistic alterations-is triggered by nonlinear dynamic interactions of genetic/epigenetic and environmental risk factors, which, ultimately, converge into a biologically heterogeneous disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ) is a key protein in Alzheimer's disease (AD) in that its accumulation induces complex pathological changes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A plethora of dynamic pathophysiological mechanisms underpins highly heterogeneous phenotypes in the field of dementia, particularly in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease without a cure. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The expression of microRNA (miRNA) is influenced by ongoing biological processes, including aging, and has begun to play a role in the measurement of neurodegenerative processes in central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A European working group has provided a new set of recommendations for the use of cerebrospinal fluid (CSF) biomarkers in the diagnostic evaluation of Alzheimer disease and mild cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
CSF Aβ42, total tau (t-tau) and phosphorylated tau (p-tau) significantly differed across the three groups. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In recent years, the idea that sleep is critical for cognitive processing has gained strength. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Identification of neurodegeneration-monitoring biomarkers would be of great clinical value for Alzheimer's disease (AD) diagnosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With increasing prevalence of Alzheimer's disease (AD) and advances in research of therapeutic approaches, an early and accurate in-vivo diagnosis is crucial. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Specific changes in personality profiles may represent early non-cognitive symptoms of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease affecting the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,322 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.
- Maternal family history is associated with Alzheimer's disease biomarkers
- Reduced CSF p-Tau181 to Tau ratio is a biomarker for FTLD-TDP
- Effects of time of the day at sampling on CSF and plasma levels of Alzheimer' disease biomarkers
- Biomarker-Based Prediction of Longitudinal Tau Positron Emission Tomography in Alzheimer Disease
- Anxiety is related to Alzheimer cerebrospinal fluid markers in subjects with mild cognitive impairment
- Cerebrospinal fluid tau protein levels in schizophrenia
- Stable isotope labelling kinetics of neurofilament light
- Cognitive Phenotyping and Interpretation of Alzheimer Blood Biomarkers
- Metallothionein-I-II and GFAP positivity in the brains from frontotemporal dementia patients
- N-myc and c-myc expression in Alzheimer disease, Huntington disease and Parkinson disease
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 →