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

Insulin and IGF-1 regularize energy metabolites in neural cells expressing full-length mutant huntingtin.

Neuropeptides - 1 Aug 2016

Naia Luana, Ribeiro Márcio, Rodrigues Joana, Duarte Ana I, Lopes Carla, Rosenstock Tatiana R, Hayden Michael R, Rego A Cristina

Abstract excerpt

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder linked to the expression of mutant huntingtin. Bioenergetic dysfunction has been described to contribute to HD pathogenesis. Thus, treatment paradigms aimed to ameliorate energy deficits appear to be suitable candidates in HD. In previous studies, we observed protective effects of insulin growth factor-1 (IGF-1) in YAC128 and R6/2 mice,...

Read the complete abstract on PubMed

Topics

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

Share to Cerebral Cortex
Share to Corpus Striatum

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Energy Metabolism

Share to Gene Knock-In Techniques

Share to Huntingtin Protein

Share to Huntington Disease

Share to Insulin

Share to Insulin-Like Growth Factor I

Source

Identifiers

PMID: 26876526
DOI: 10.1016/j.npep.2016.01.009

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

Insulin and IGF-1 regularize energy metabolites in neural cells expressing full-length mutant huntingtin.PMID 26876526Read ↗

Oxidative metabolism in YAC128 mouse model of Huntington's disease.Semantic proximity Read ↗

Energy deficit in Huntington disease: why it mattersSemantic proximity Read ↗

Mitochondrial dysfunction in Huntington's disease: the bioenergetics of isolated and in situ mitochondria from transgenic mice.Semantic proximity Read ↗

Energy dysfunction in Huntington’s disease: insights from PGC-1α, AMPK, and CKBSemantic proximity Read ↗

Targeting energy metabolism in Huntington's disease.Semantic proximity Read ↗

Requirement for oxidation of neuronal ketone bodies in aging and neurodegenerationSemantic proximity Read ↗

IGF-1 intranasal administration rescues Huntington's disease phenotypes in YAC128 mice.Semantic proximity Read ↗

Neurons undergo pathogenic metabolic reprograming in models of familial ALSSemantic proximity Read ↗

Superoxide dismutase 1 mutation in a cellular model of amyotrophic lateral sclerosis shifts energy generation from oxidative phosphorylation to glycolysis.Semantic proximity Read ↗

Inhibitors of metabolism rescue cell death in Huntington's disease models.Semantic proximity Read ↗

HD CAG repeat implicates a dominant property of huntingtin in mitochondrial energy metabolism.Semantic proximity Read ↗

Enhanced activity of glycolytic enzymes in <i>Drosophila</i> and human cell models of Parkinson’s disease based on <i>DJ-1</i> deficiencySemantic proximity Read ↗

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