ArticleFrontiers in molecular neuroscience2018
Overexpression of Wild-Type Human Alpha-Synuclein Causes Metabolism Abnormalities in Thy1-aSYN Transgenic Mice.
Article in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 47 citations in OpenAlex.
- Glycerol 3-phosphate acyltransferase exacerbates α-synuclein-induced toxicity by increasing lipid peroxidation.Nature communications · 2026Article
- Inter-Organ Crosstalk in Neurodegenerative Disease.Life (Basel, Switzerland) · 2025Review
- The genomics of the domestication syndrome in a songbird model species.Communications biology · 2025Article
- Metabolic dysregulation and resistance to high-fat diet-induced weight gain in mice overexpressing human wild-type α-synuclein.NPJ Parkinson's disease · 2025Article
- Assessment of Neurobehavioral Performance and Markers of Synaptic Vesicle Trafficking in an Alpha-Synuclein Knockout Mouse Model after Controlled Cortical Impact Injury.Neurotrauma reports · 2025Article
- Review
- α-synuclein overexpression and the microbiome shape the gut and brain metabolome in mice.NPJ Parkinson's disease · 2024Article
- Review
- Alpha-synuclein-induced stress sensitivity renders the Parkinson's disease brain susceptible to neurodegeneration.Acta neuropathologica communications · 2024Article
- α-Synuclein Overexpression and the Microbiome Shape the Gut and Brain Metabolome in Mice.bioRxiv : the preprint server for biology · 2024Article
- A Mouse Model to Test Novel Therapeutics for Parkinson's Disease: an Update on the Thy1-aSyn ("line 61") Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- α-Synuclein at the Presynaptic Axon Terminal as a Double-Edged Sword.Biomolecules · 2022Review
- Sleep and circadian rhythms in Parkinson's disease and preclinical models.Molecular neurodegeneration · 2022Review
- Potential Crosstalk Between Parkinson's Disease and Energy Metabolism.Aging and disease · 2021Review
- Behavioral Deficits and Brain α-Synuclein and Phosphorylated Serine-129 α-Synuclein in Male and Female Mice Overexpressing Human α-Synuclein.Journal of Alzheimer's disease : JAD · 2021Article
- Alpha-Synuclein Pathology Coincides With Increased Number of Early Stage Neural Progenitors in the Adult Hippocampus.Frontiers in cell and developmental biology · 2021Article
- TULP2, a New RNA-Binding Protein, Is Required for Mouse Spermatid Differentiation and Male Fertility.Frontiers in cell and developmental biology · 2021Article
- Overexpression of an ALS-associated FUS mutation inBiology open · 2020Article
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Authors and funding
20 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease is a progressive neurodegenerative disorder characterized by loss of dopaminergic neurons, pathological accumulation of alpha-synuclein and motor symptoms, but also by non-motor symptoms. Metabolic abnormalities including body weight loss have been reported in patients and could precede by several years the emergence of classical motor manifestations. However, our understanding of the pathophysiological mechanisms underlying body weight loss in PD is limited. The present study investigated the links between alpha-synuclein accumulation and energy metabolism in transgenic mice overexpressing Human wild-type (WT) alpha-synuclein under the Thy1 promoter (Thy1-aSYN mice). Results showed that Thy1-aSYN mice gained less body weight throughout life than WT mice, with significant difference observed from 3 months of age. Body composition analysis of 6-month-old transgenic animals showed that body mass loss was due to lower adiposity. Thy1-aSYN mice displayed lower food consumption, increased spontaneous activity, as well as a reduced energy expenditure compared to control mice. While no significant change in glucose or insulin responses were observed, Thy1-aSYN mice had significantly lower plasmatic levels of insulin and leptin than control animals. Moreover, the pathological accumulation of alpha-synuclein in the hypothalamus of 6-month-old Thy1-aSYN mice was associated with a down-regulation of the phosphorylated active form of the signal transducer and activator of transcription 3 (STAT3) and of Rictor (the mTORC2 signaling pathway), known to couple hormonal signals with the maintenance of metabolic and energy homeostasis. Collectively, our results suggest that (i) metabolic alterations are an important phenotype of alpha-synuclein overexpression in mice and that (ii) impaired STAT3 activation and mTORC2 levels in the hypothalamus may underlie the disruption of feeding regulation and energy metabolism in Thy1-aSYN mice.
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