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Dynamic metabolic patterns tracking neurodegeneration and gliosis following 26S proteasome dysfunction in mouse forebrain neurons.
Geiszler, Philippine C; Ugun-Klusek, Aslihan; Lawler, Karen; Pardon, Marie-Christine; Yuchun, Ding; Bai, Li; Daykin, Clare A; Auer, Dorothee P; Bedford, Lynn.
Afiliación
  • Geiszler PC; Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham, UK.
  • Ugun-Klusek A; School of Pharmacy, University of Nottingham, Nottingham, UK.
  • Lawler K; School of Science and Technology, Nottingham Trent University, Nottingham, UK.
  • Pardon MC; School of Life Sciences, University of Nottingham, Nottingham, UK.
  • Yuchun D; School of Life Sciences, University of Nottingham, Nottingham, UK.
  • Bai L; School of Computing, University of Newcastle, Newcastle, UK.
  • Daykin CA; School of Computer Sciences, University of Nottingham, Nottingham, UK.
  • Auer DP; School of Pharmacy, University of Nottingham, Nottingham, UK.
  • Bedford L; Metaboconsult UK, Heanor, Derbyshire, UK.
Sci Rep ; 8(1): 4833, 2018 03 19.
Article en En | MEDLINE | ID: mdl-29555943
Metabolite profiling is an important tool that may better capture the multiple features of neurodegeneration. With the considerable parallels between mouse and human metabolism, the use of metabolomics in mouse models with neurodegenerative pathology provides mechanistic insight and ready translation into aspects of human disease. Using 400 MHz nuclear magnetic resonance spectroscopy we have carried out a temporal region-specific investigation of the metabolome of neuron-specific 26S proteasome knockout mice characterised by progressive neurodegeneration and Lewy-like inclusion formation in the forebrain. An early significant decrease in N-acetyl aspartate revealed evidence of neuronal dysfunction before cell death that may be associated with changes in brain neuroenergetics, underpinning the use of this metabolite to track neuronal health. Importantly, we show early and extensive activation of astrocytes and microglia in response to targeted neuronal dysfunction in this context, but only late changes in myo-inositol; the best established glial cell marker in magnetic resonance spectroscopy studies, supporting recent evidence that additional early neuroinflammatory markers are needed. Our results extend the limited understanding of metabolite changes associated with gliosis and provide evidence that changes in glutamate homeostasis and lactate may correlate with astrocyte activation and have biomarker potential for tracking neuroinflammation.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Prosencéfalo / Complejo de la Endopetidasa Proteasomal / Metabolómica / Gliosis / Neuronas Límite: Animals Idioma: En Revista: Sci Rep Año: 2018 Tipo del documento: Article Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Prosencéfalo / Complejo de la Endopetidasa Proteasomal / Metabolómica / Gliosis / Neuronas Límite: Animals Idioma: En Revista: Sci Rep Año: 2018 Tipo del documento: Article Pais de publicación: Reino Unido