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Find studies

Showing 126–149 of 149 studies with an author at Institut du Cerveau (FR) (page 6 of 6) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 149 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.

Positron emission tomography (PET) imaging of brain amyloid beta is now clinically available in several countries including the United States and the United Kingdom, but not Canada. 1 key finding →

Evidence: low

We found 5 distinct clusters of subjects (N=38, N=16, N=24, N=14, N=21) with a composition statistically independent from that obtained using available clinical diagnostic criteria (each cluster included all phenotypical groups). 3 key findings →

Participants: 20 Evidence: moderate

Cognitive assessment and analysis of plasma biomarkers are lower-cost options for the early assessment of Alzheimer's disease (AD). 1 key finding →

Participants: 327 Evidence: low

Individual biomarkers significantly predict decline across multiple cognitive domains. 5 key findings →

Evidence: low

In total, 24 recommendations were developed covering the research landscape and priorities within research in AD following a possible approval, potential impact on health care systems and diagnostic pathways, and communication to patients about anti-amyloid antibodies. 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

We dissociated four key cognitive components underlying remote thinking: spontaneous associative thinking, inhibition of unoriginal responses, intentional remote associative thinking, and verbal initiation; and replicated them in three independent datasets. 5 key findings →

Evidence: low

Caspase cleaved amyloid precursor protein (APPcc) and SET are increased and mislocalized in the neuronal cytoplasm in Alzheimer Disease (AD) brains. 1 key finding →

Evidence: low

We have successfully generated specific high affinity monoclonal antibodies against p -Tau217, p -Tau205, and N-terminus GFAP and have confirmed that these antibodies have the necessary specificity and sensitivity for the Simoa platform. 2 key findings →

Evidence: moderate

In the last decade, a number of important research advances in different fields have allowed Down syndrome (DS) research to flourish, creating a time of both unparalleled opportunity and considerable challenge. 1 key finding →

Evidence: low

SET is a multifunctional protein, but when present in the cytoplasm, acts as a powerful inhibitor of phosphatase 2A. We previously observed that in CA1 of Down syndrome (DS) patients, the level of SET is increased, and SET is translocated to the cytoplasm and associated with the hyperphosphorylation of tau at ser202/thr205. 2 key findings →

Evidence: low

Cerebral small vessel disease can manifest as vascular dementia, typically associated with vascular risk factors or cerebral amyloid angiopathy, and more rarely associated with hereditary conditions. 5 key findings →

Evidence: low

Autosomal dominant Alzheimer disease (ADAD) is caused by pathogenic variants in the APP, PSEN1 and PSEN2 genes, but a substantial fraction of reported variants is of unknown clinical significance. 4 key findings →

Evidence: low

For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). 3 key findings →

Evidence: low

The locus of the gene PTK2B encoding the tyrosine kinase Pyk2 has been associated with the risk of late-onset Alzheimer’s disease, the predominant form of dementia. 3 key findings →

Evidence: low

A head-to-head comparison of plasma biomarkers to detect biologically defined Alzheimer in a memory clinic

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2024-10-27

Blood-based biomarkers for Alzheimer’s disease (AD) have been widely studied, but direct comparisons of several biomarkers in clinical settings remain limited. 4 key findings →

Design: cross-sectional Participants: 197 Evidence: moderate

GCH1 genetic variation as a prognostic factor in Parkinsons disease across populations

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-19

BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →

Design: longitudinal study Participants: 22,825 Evidence: moderate

Multi-trait Polygenic Profiling and Survival Free of Dementia and Disability: Results from the Health and Retirement Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-11

ObjectiveTo determine whether a multi-trait polygenic profile for dementia is associated with dementia- and disability-free survival in middle-aged and older adults. 5 key findings →

Design: longitudinal study Evidence: moderate

Pathway-specific polygenic risk scores reveal underlying mechanisms of cerebral small vessel disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-14

White matter hyperintensities (WMH), a key MRI-marker of cerebral small vessel disease (cSVD), are common in older adults and associated with an increased risk of stroke and dementia. 5 key findings →

Participants: 46,944 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
  • Randomized / 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
  • Multicenter 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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    Where this research is being discussed: events