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

A combination drug therapy improves cognition and reverses gene expression changes in a mouse model of Huntington's disease.

The European journal of neuroscience - 1 Feb 2005

Morton A Jennifer, Hunt Mark J, Hodges Angela K, Lewis Paul D, Redfern Amanda J, Dunnett Stephen B, Jones Lesley

Abstract excerpt

Huntington's disease is a genetic disease caused by a single mutation. It is characterized by progressive movement, emotional and cognitive deficits. R6/2 mice transgenic for exon 1 of the HD gene with 150+ CAG repeats have a progressive neurological phenotype, including deterioration in cognitive function. The mechanism underlying the cognitive deficits in R6/2 mice is unknown, but dysregulated gene expression,...

Read the complete abstract on PubMed

Topics

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

Share to Brain Chemistry
Share to Cognition Disorders

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Huntington Disease

Share to Maze Learning

Share to Neurotransmitter Agents

Share to Rotarod Performance Test

Share to Spatial Behavior

Share to Trinucleotide Repeats

Source

Identifiers

PMID: 15787692
DOI: 10.1111/j.1460-9568.2005.03895.x

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A combination drug therapy improves cognition and reverses gene expression changes in a mouse model of Huntington's disease.PMID 15787692Read ↗

Up-regulation of GLT1 expression increases glutamate uptake and attenuates the Huntington's disease phenotype in the R6/2 mouse.Semantic proximity Read ↗

Calcineurin inhibitors cause an acceleration of the neurological phenotype in a mouse transgenic for the human Huntington's disease mutation.Semantic proximity Read ↗

Dodecyl Creatine Ester Improves Cognitive Function and Identifies Drivers of Creatine DeficiencySemantic proximity Read ↗

Dysregulation of gene expression in the R6/2 model of polyglutamine disease: parallel changes in muscle and brainSemantic proximity Read ↗

Selective inhibition of histone deacetylase 1 and 3 improves motor phenotype and alleviates transcriptional dysregulation in Huntington’s disease miceSemantic proximity Read ↗

A small molecule p75NTR ligand normalizes signalling and reduces Huntington's disease phenotypes in R6/2 and BACHD mice.Semantic proximity Read ↗

Environmental enrichment slows disease progression in R6/2 Huntington's disease mice.Semantic proximity Read ↗

Chronic cholesterol administration to the brain supports complete and long-lasting cognitive and motor amelioration in Huntington’s diseaseSemantic proximity Read ↗

SAHA decreases HDAC 2 and 4 levels in vivo and improves molecular phenotypes in the R6/2 mouse model of Huntington's disease.Semantic proximity Read ↗

The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntington's disease transgenic mice.Semantic proximity Read ↗

Chronic lithium chloride treatment has variable effects on motor behaviour and survival of mice transgenic for the Huntington's disease mutation.Semantic proximity Read ↗

Depletion of Complexin II does not affect disease progression in a mouse model of Huntington's disease (HD); support for role for complexin II in behavioural pathology in a mouse model of HD.Semantic proximity Read ↗

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