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

Structural and molecular myelination deficits occur prior to neuronal loss in the YAC128 and BACHD models of Huntington disease

28 Apr 2016

Abstract excerpt

White matter (WM) atrophy is a significant feature of Huntington disease (HD), although its aetiology and early pathological manifestations remain poorly defined. In this study, we aimed to characterize WM-related features in the transgenic YAC128 and BACHD models of HD. Using diffusion tensor magnetic resonance imaging (DT-MRI), we demonstrate that microstructural WM abnormalities occur from an early age in...

Read the complete abstract on PubMed

Topics

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

Share to Genetic Neurodegenerative Diseases
Share to Mitochondrial Function and Pathology
Share to Parkinson's Disease Mechanisms and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 27126634
DOI: 10.1093/hmg/ddw122

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Structural and molecular myelination deficits occur prior to neuronal loss in the YAC128 and BACHD models of Huntington diseasePMID 27126634Read ↗

Marked differences in neurochemistry and aggregates despite similar behavioural and neuropathological features of Huntington disease in the full-length BACHD and YAC128 miceSemantic proximity Read ↗

Comparative analysis of pathology and behavioural phenotypes in mouse models of Huntington's disease.Semantic proximity Read ↗

Loss of wild-type huntingtin influences motor dysfunction and survival in the YAC128 mouse model of Huntington diseaseSemantic proximity Read ↗

Selective striatal neuronal loss in a YAC128 mouse model of Huntington disease.Semantic proximity Read ↗

Early white matter abnormalities, progressive brain pathology and motor deficits in a novel knock-in mouse model of Huntington's disease.Semantic proximity Read ↗

Levels of mutant huntingtin influence the phenotypic severity of Huntington disease in YAC128 mouse models.Semantic proximity Read ↗

Selective degeneration and nuclear localization of mutant huntingtin in the YAC128 mouse model of Huntington disease.Semantic proximity Read ↗

Early reduction and impaired targeting of myelin-associated glycoprotein to myelin membranes in Huntington’s diseaseSemantic proximity Read ↗

Manipulation of microbiota reveals altered myelination and white matter plasticity in a model of Huntington diseaseSemantic proximity Read ↗

Phenotypic abnormalities in the YAC128 mouse model of Huntington disease are penetrant on multiple genetic backgrounds and modulated by strain.Semantic proximity Read ↗

White matter changes in Huntington’s disease and the demyelination hypothesis: a critical reviewSemantic proximity Read ↗

Age-dependent alterations of the kynurenine pathway in the YAC128 mouse model of Huntington disease.Semantic proximity Read ↗

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