Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Overexpression of DYRK1A inhibits choline acetyltransferase induction by oleic acid in cellular models of Down syndrome.

Experimental neurology - 1 Jan 2013

Hijazi Maruan, Fillat Cristina, Medina José M, Velasco Ana

Abstract excerpt

Histological brain studies of individuals with DS have revealed an aberrant formation of the cerebral cortex. Previous work from our laboratory has shown that oleic acid acts as a neurotrophic factor and induces neuronal differentiation. In order to characterize the effects of oleic acid in a cellular model of DS, immortalized cell lines derived from the cortex of trisomy Ts16 (CTb) and normal mice (CNh) were...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Choline O-Acetyltransferase
Share to Down Syndrome

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Dyrk Kinases

Share to Enzyme Induction

Share to Nerve Growth Factors

Share to Oleic Acid

Share to Protein-Tyrosine Kinases

Share to Trisomy

Source

Identifiers

PMID: 23124096
DOI: 10.1016/j.expneurol.2012.10.016

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 9 closest

Overexpression of DYRK1A inhibits choline acetyltransferase induction by oleic acid in cellular models of Down syndrome.PMID 23124096Read ↗

Targeting trisomic treatments: optimizing Dyrk1a inhibition to improve Down syndrome deficitsSemantic proximity Read ↗

Epigallocatechin‐3‐gallate, a DYRK1A inhibitor, rescues cognitive deficits in <scp>D</scp>own syndrome mouse models and in humansSemantic proximity Read ↗

Dyrk1A overexpression in immortalized hippocampal cells produces the neuropathological features of Down syndromeSemantic proximity Read ↗

Prenatal treatment with EGCG enriched green tea extract rescues GAD67 related developmental and cognitive defects in Down syndrome mouse modelsSemantic proximity Read ↗

<i>Cbs</i> overdosage is necessary and sufficient to induce cognitive phenotypes in mouse models of Down syndrome and interacts genetically with <i>Dyrk1a</i>Semantic proximity Read ↗

Septal cell lines derived from the trisomy 16 mouse: generation, characterization, and response to NGF.Semantic proximity Read ↗

Role of Trisomy 21 Mosaicism in Sporadic and Familial Alzheimer's DiseaseSemantic proximity Read ↗

Trisomy-driven overexpression of DYRK1A kinase in the brain of subjects with Down syndromeSemantic proximity Read ↗

DYRK1A, a novel determinant of the methionine-homocysteine cycle in different mouse models overexpressing this Down-syndrome-associated kinase.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.