ArticleHuman molecular genetics2014
Genetically altering organismal metabolism by leptin-deficiency benefits a mouse model of amyotrophic lateral sclerosis.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Leptin: role over central nervous system in epilepsy.BMC neuroscience · 2018Pooled it
- Review
- Leptin haploinsufficiency exerts sex-dependent partial protection in SOD1Scientific reports · 2024Article
- Loss of hypothalamic MCH decreases food intake in amyotrophic lateral sclerosis.Acta neuropathologica · 2023Article
- Ozone modified hypothalamic signaling enhancing thermogenesis in the TDP-43Scientific reports · 2022Article
- Alterations in metabolic biomarkers and their potential role in amyotrophic lateral sclerosis.Annals of clinical and translational neurology · 2022Article
- Metabolic Profile and Pathological Alterations in the Muscle of Patients with Early-Stage Amyotrophic Lateral Sclerosis.Biomedicines · 2022Article
- The potential benefit of leptin therapy against amyotrophic lateral sclerosis (ALS).Brain and behavior · 2022Article
- Food for Thought: Leptin and Hippocampal Synaptic Function.Frontiers in pharmacology · 2022Review
- Alterations in Leptin Signaling in Amyotrophic Lateral Sclerosis (ALS).International journal of molecular sciences · 2021Article
- Disruption of orbitofrontal-hypothalamic projections in a murine ALS model and in human patients.Translational neurodegeneration · 2021Article
- The links between diabetes mellitus and amyotrophic lateral sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Review
- Altered expression of clock and clock-controlled genes in a hSOD1-linked amyotrophic lateral sclerosis mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- The Neuronal Actions of Leptin and the Implications for Treating Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Brain energy rescue: an emerging therapeutic concept for neurodegenerative disorders of ageing.Nature reviews. Drug discovery · 2020Review
- The effects of diet and sex in amyotrophic lateral sclerosis.Revue neurologique · 2020Review
- Eating peptides: biomarkers of neurodegeneration in amyotrophic lateral sclerosis and frontotemporal dementia.Annals of clinical and translational neurology · 2019Article
- Defective daily temperature regulation in a mouse model of amyotrophic lateral sclerosis.Experimental neurology · 2019Article
- Genetic induction of hypometabolism by ablation of MC4R does not suppress ALS-like phenotypes in the G93A mutant SOD1 mouse model.Scientific reports · 2017Article
- Adipokines, C-reactive protein and Amyotrophic Lateral Sclerosis - results from a population- based ALS registry in Germany.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal, neurodegenerative disease that causes death of motor neurons. ALS patients and mouse models of familial ALS display organismal level metabolic dysfunction, which includes increased energy expenditure despite decreased lean mass. The pathophysiological relevance of abnormal energy homeostasis to motor neuron disease remains unclear. Leptin is an adipocyte-derived hormone that regulates whole-animal energy expenditure. Here, we report that placing mutant superoxide dismutase 1 (SOD1) mice in a leptin-deficient background improves energy homeostasis and slows disease progression. Leptin-deficient mutant SOD1 mice possess increased bodyweight and fat mass, as well as decreased energy expenditure. These observations coincide with enhanced survival, improved strength and decreased motor neuron loss. These results suggest that altering whole-body energy metabolism in mutant SOD1 mice can mitigate disease progression. We propose that manipulations that increase fat mass and reduce energy expenditure will be beneficial in the setting of motor neuron disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.