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

Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice.

Proceedings of the National Academy of Sciences of the United States of America - 4 Mar 2003

Duan Wenzhen, Guo Zhihong, Jiang Haiyang, Ware Melvin, Li Xiao-Jiang, Mattson Mark P

Abstract excerpt

In addition to neurological deficits, Huntington's disease (HD) patients and transgenic mice expressing mutant human huntingtin exhibit reduced levels of brain-derived neurotrophic factor, hyperglycemia, and tissue wasting. We show that the progression of neuropathological (formation of huntingtin inclusions and apoptotic protease activation), behavioral (motor dysfunction), and metabolic (glucose intolerance and...

Read the complete abstract on PubMed

Topics

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

Share to Blood Glucose
Share to Brain-Derived Neurotrophic Factor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Caspases

Share to Glucose

Share to Huntingtin Protein

Share to Immunoblotting

Share to Leptin

Share to Neurodegenerative Diseases

Source

Open in PubMed Open full text

Identifiers

PMID: 12589027
DOI: 10.1073/pnas.0536856100
PMCID: PMC151440

Genes

BDNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice.PMID 12589027Read ↗

Customized Dietary Intervention Avoids Unintentional Weight Loss and Modulates Circulating miRNAs Footprint in Huntington's DiseaseSemantic proximity Read ↗

Early energy deficit in Huntington disease: identification of a plasma biomarker traceable during disease progression.Semantic proximity Read ↗

Curcumin dietary supplementation ameliorates disease phenotype in an animal model of Huntington’s disease.Semantic proximity Read ↗

The role of calorie restriction and SIRT1 in prion-mediated neurodegenerationSemantic proximity Read ↗

PGC-1α rescues Huntington's disease proteotoxicity by preventing oxidative stress and promoting TFEB function.Semantic proximity Read ↗

Huntington's disease.Semantic proximity Read ↗

Thermoregulatory and metabolic defects in Huntington's disease transgenic mice implicate PGC-1α in Huntington's disease neurodegenerationSemantic proximity Read ↗

Reinstating aberrant mTORC1 activity in Huntington's disease mice improves disease phenotypes.Semantic proximity Read ↗

Weight loss in Huntington disease increases with higher CAG repeat numberSemantic proximity Read ↗

Effects of age and dietary methionine restriction on cognitive and behavioural phenotypes in the rTg4510 mouse model of frontotemporal dementia.Semantic proximity Read ↗

Hypothalamic expression of huntingtin causes distinct metabolic changes in Huntington's disease mice.Semantic proximity Read ↗

Mutant huntingtin causes metabolic imbalance by disruption of hypothalamic neurocircuits.Semantic proximity Read ↗

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