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January 19, 2023
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Modulating SIRT1 in astrocytes: A potential treatment for neurodegenerative diseases
Recent research analyzed the influence of SIRT1 on astrocytes and its potential as a CNS-specific therapy for multiple sclerosis. It presented significant results.
Astrocytes are cells in the central nervous system (CNS) that have several functions, like neural signal transmission, supporting neural and glial cell survival, and maintaining the integrity of the blood-brain barrier (BBB). These cells have mixed roles in multiple sclerosis (MS). Following a spinal cord injury, an astrocyte scar supports CNS axon regeneration. Astrocytes also produce neurotrophic factors that promote oligodendrocyte maturation and remyelination. On the other hand, astrocytes surrounding MS lesions release proinflammatory mediators during CNS inflammation that increase BBB permeability and leukocyte recruitment. Advances in molecular techniques have allowed the mapping of several astrocyte subsets. Understanding astrocyte heterogeneity could help identify therapeutic approaches that switch pathogenic subsets to beneficial ones in conditions like MS.
Sirtuins (SIRTs) are a family of protein deacetylases that play significant roles in the cell cycle, senescence, inflammation, and metabolism. SIRT1, a member of the SIRTs family, has been found to act as an epigenetic modulator with mixed pro- and anti-inflammatory roles. In animal models, T-cell SIRT1 deletion protected mice from experimental autoimmune encephalomyelitis (EAE). EAE is a preclinical model of CNS inflammatory demyelinating disease. The role of SIRT1 in astrocytes remains controversial, and in the case of MS/EAE it is unknown.
In their study, Zhang et al. sought to define SIRT1 influence on astrocytes and explore the potential of SIRT1 targeting in these cells as a CNS-specific therapy for MS. Their experimental model consisted of several mice breeds.
The results revealed that reactive astrocytes (astrocytes that undergo morphological, functional, and molecular remodeling in response to pathological factors) expressed high SIRT1 levels, displayed neurotoxic properties, and caused CNS demyelination. Furthermore, SIRT1 inactivation in astrocytes inhibited proinflammatory mediators’ production and converted these cells into a glioprotective phenotype. In addition, SIRT1 genetic deletion effectively inhibited EAE progression.
The authors concluded that their findings highlight a novel technique that could switch pathological astrocytes into beneficial ones, supporting the development of astrocyte-targeting therapies for conditions like MS. Nevertheless, further research is needed to explore this potential technique in other preclinical models. Years of research still lie ahead before such a technology could be considered for clinical evaluation.
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Astrocytes are cells in the central nervous system (CNS) that have several functions, like neural signal transmission, supporting neural and glial cell survival, and maintaining the integrity of the blood-brain barrier (BBB). These cells have mixed roles in multiple sclerosis (MS). Following a spinal cord injury, an astrocyte scar supports CNS axon regeneration. Astrocytes also produce neurotrophic factors that promote oligodendrocyte maturation and remyelination. On the other hand, astrocytes surrounding MS lesions release proinflammatory mediators during CNS inflammation that increase BBB permeability and leukocyte recruitment. Advances in molecular techniques have allowed the mapping of several astrocyte subsets. Understanding astrocyte heterogeneity could help identify therapeutic approaches that switch pathogenic subsets to beneficial ones in conditions like MS.
Sirtuins (SIRTs) are a family of protein deacetylases that play significant roles in the cell cycle, senescence, inflammation, and metabolism. SIRT1, a member of the SIRTs family, has been found to act as an epigenetic modulator with mixed pro- and anti-inflammatory roles. In animal models, T-cell SIRT1 deletion protected mice from experimental autoimmune encephalomyelitis (EAE). EAE is a preclinical model of CNS inflammatory demyelinating disease. The role of SIRT1 in astrocytes remains controversial, and in the case of MS/EAE it is unknown.
In their study, Zhang et al. sought to define SIRT1 influence on astrocytes and explore the potential of SIRT1 targeting in these cells as a CNS-specific therapy for MS. Their experimental model consisted of several mice breeds.
The results revealed that reactive astrocytes (astrocytes that undergo morphological, functional, and molecular remodeling in response to pathological factors) expressed high SIRT1 levels, displayed neurotoxic properties, and caused CNS demyelination. Furthermore, SIRT1 inactivation in astrocytes inhibited proinflammatory mediators’ production and converted these cells into a glioprotective phenotype. In addition, SIRT1 genetic deletion effectively inhibited EAE progression.
The authors concluded that their findings highlight a novel technique that could switch pathological astrocytes into beneficial ones, supporting the development of astrocyte-targeting therapies for conditions like MS. Nevertheless, further research is needed to explore this potential technique in other preclinical models. Years of research still lie ahead before such a technology could be considered for clinical evaluation.
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Dr. Ana Baroni MD. Ph.D.
Scientific & Medical Advisor
Quality Garant
Ana has over 20 years of consultancy experience in longevity, regenerative and precision medicine. She has a multifaceted understanding of genomics, molecular biology, clinical biochemistry, nutrition, aging markers, hormones and physical training. This background allows her to bridge the gap between longevity basic sciences and evidence-based real interventions, putting them into the clinic, to enhance the healthy aging of people. She is co-founder of Origen.life, and Longevityzone. Board member at Breath of Health, BioOx and American Board of Clinical Nutrition. She is Director of International Medical Education of the American College of Integrative Medicine, Professor in IL3 Master of Longevity at Barcelona University and Professor of Nutrigenomics in Nutrition Grade in UNIR University.
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