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Beyond Motor Deficits: Environmental Enrichment Mitigates Huntington's Disease Effects in YAC128 Mice.
Plácido, Evelini; Gomes Welter, Priscilla; Wink, Ana; Karasiak, Gabriela Duarte; Outeiro, Tiago Fleming; Dafre, Alcir Luiz; Gil-Mohapel, Joana; Brocardo, Patricia S.
Afiliação
  • Plácido E; Neuroscience Graduate Program, Center of Biological Sciences, Federal University of Santa Catarina, Florianopolis 88040-900, SC, Brazil.
  • Gomes Welter P; Neuroscience Graduate Program, Center of Biological Sciences, Federal University of Santa Catarina, Florianopolis 88040-900, SC, Brazil.
  • Wink A; Neuroscience Graduate Program, Center of Biological Sciences, Federal University of Santa Catarina, Florianopolis 88040-900, SC, Brazil.
  • Karasiak GD; Department of Biochemistry, Center of Biological Sciences, Federal University of Santa Catarina, Florianopolis 88040-900, SC, Brazil.
  • Outeiro TF; Department of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Göttingen, 37075 Göttingen, Germany.
  • Dafre AL; Max Planck Institute for Natural Sciences, 37075 Göttingen, Germany.
  • Gil-Mohapel J; Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Framlington Place, Newcastle Upon Tyne NE1 7RU, UK.
  • Brocardo PS; Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), 18147 Göttingen, Germany.
Int J Mol Sci ; 24(16)2023 Aug 09.
Article em En | MEDLINE | ID: mdl-37628801
Huntington's disease (HD) is a neurodegenerative genetic disorder characterized by motor, psychiatric, cognitive, and peripheral symptoms without effective therapy. Evidence suggests that lifestyle factors can modulate disease onset and progression, and environmental enrichment (EE) has emerged as a potential approach to mitigate the progression and severity of neurodegenerative processes. Wild-type (WT) and yeast artificial chromosome (YAC) 128 mice were exposed to different EE conditions. Animals from cohort 1 were exposed to EE between postnatal days 21 and 60, and animals from cohort 2 were exposed to EE between postnatal days 60 and 120. Motor and non-motor behavioral tests were employed to evaluate the effects of EE on HD progression. Monoamine levels, hippocampal cell proliferation, neuronal differentiation, and dendritic arborization were also assessed. Here we show that EE had an antidepressant-like effect and slowed the progression of motor deficits in HD mice. It also reduced monoamine levels, which correlated with better motor performance, particularly in the striatum. EE also modulated neuronal differentiation in the YAC128 hippocampus. These results confirm that EE can impact behavior, hippocampal neuroplasticity, and monoamine levels in YAC128 mice, suggesting this could be a therapeutic strategy to modulate neuroplasticity deficits in HD. However, further research is needed to fully understand EE's mechanisms and long-term effects as an adjuvant therapy for this debilitating condition.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doença de Huntington / Transtornos Heredodegenerativos do Sistema Nervoso Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Int J Mol Sci Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Brasil País de publicação: Suíça

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doença de Huntington / Transtornos Heredodegenerativos do Sistema Nervoso Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Int J Mol Sci Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Brasil País de publicação: Suíça