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Find studies

Showing 176–200 of 201 studies with an author at Amsterdam University Medical Centers (NL) (page 8 of 9) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 201 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Our results indicate that decline in semantic fluency is an early indicator of cognitive deficits in preclinical Alzheimer's disease. 5 key findings →

Participants: 490 Evidence: low

Three subtypes emerged: severe obesity-related inflammatory diabetes (SOID), mild metabolic diabetes (MMD, reference), and mild age-related hypertension-predominant diabetes (MARD-H). 5 key findings →

Evidence: low

Dementia with Lewy bodies (DLB), a progressive neurodegenerative disease with heterogeneous clinical presentations, greatly impacts patients, caregivers, and society. 5 key findings →

Evidence: low

Deciding on genetic testing for familial dementia: Perspectives of patients and families

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Alzheimer s & Dementia 2025-04-01

Of 138 (27%) eligible patients (46% female, age 61 ± 8 years, Mini-Mental State Examination [MMSE] 22 ± 6), 75 (54%) underwent genetic testing. 5 key findings →

Participants: 15 Evidence: low

AcTau174 levels were elevated in all dementia groups compared to controls, with a stepwise increase from controls to MCI-AD (2.2-fold) to AD dementia (3.5-fold, Figure 1). 5 key findings →

Evidence: moderate

Vascular burden influences NfL levels, particularly in A- individuals at a symptomatic stage. 5 key findings →

Design: cross-sectional Participants: 421 Evidence: moderate

Artificial intelligence and neuroimaging enable accurate dementia prediction but often involve 'black box' models that can be difficult to trust. 5 key findings →

Evidence: low

Accurate diagnosis of frontotemporal dementia (FTD) with right anterior temporal lobe (RATL) predominance remains challenging due to lack of clinical characterization, and standardized terminology. 4 key findings →

Evidence: low

The ASURE trial design is discussed, with a particular focus on fluid biomarkers, EEG, and CFC as endpoints. 1 key finding →

Evidence: high

Onset-predictive biomarker tests (OPBTs) for genetic frontotemporal dementia (FTD) may predict symptom onset in coming years. 4 key findings →

Evidence: low

Low CSF APP refines diagnosis for p ‐tau negative Alzheimer‐like dementia

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2025-12-01

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

and neurogranin changes correlated with sabirnetug-AβO target engagement (p ≤ 0.01). 5 key findings →

Design: clinical trial Evidence: high

Synaptic loss in the (para)hippocampus is a major contributor to cognitive decline in Alzheimer's disease (AD), yet its regional specificity and pathological correlates remain poorly understood. 5 key findings →

Evidence: low

Participants’ motivations for testing and long-term adaptation to the results were strongly shaped by cognitive concerns and personal experiences of dementia in relatives. 5 key findings →

Participants: 17 Evidence: moderate

Mild cognitive impairment (MCI) is the in-between stage between healthy cognitive aging and neurodegenerative diseases such as Alzheimer's disease (AD). 5 key findings →

Evidence: low

Long-read sequencing reveals hidden structural complexity within Alzheimers disease-associated GWAS loci

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-17

Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus. 3 key findings →

Participants: 493 Evidence: low

Fine-mapping reveals four TMEM106B haplotypes associated with neurodegenerative risk and preserved cognition at extreme age

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-17

Genetic variation at the TMEM106B locus has been associated with Alzheimers disease (AD) and related neurodegenerative phenotypes, yet its haplotypic architecture remains incompletely resolved. 2 key findings →

Participants: 493 Evidence: low

Metabolomic signatures of data-driven type 2 diabetes subtypes and their associations with dementia and stroke risk

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-25

We examined whether their metabolomic profiles also differed and whether subtype-related metabolic patterns were associated with dementia, stroke, and all-cause mortality. 5 key findings →

Participants: 7,671 Evidence: low

Human leukocyte antigen (HLA) class II variation is implicated in Alzheimers disease (AD) and longevity, but its mechanisms within the major histocompatibility complex remain unclear. 2 key findings →

Participants: 6,053 Evidence: moderate

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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 →

Newest studies, as a dated timeline →    Atom feed