GIUV2026-041
Myelination was a key evolutionary event for the development of large and highly complex nervous systems in jawed vertebrates. Myelin, a lipid-rich membranous structure, enables the saltatory conduction of action potentials along axons and additionally provides metabolic support to axons through the supply of essential metabolites.
Loss of myelin, as well as alterations in its composition and organization can compromise axonal integrity and trigger neurodegenerative processes. Myelin abnormalities are a common feature of numerous central nervous system (CNS) pathologies, including leukodystrophies, spinal cord injuries, multiple sclerosis (MS) and other inflammatory demyelinating disorders of the CNS, periventricular leukomalacia, as well as several classical neurodegenerative diseases such as Alzheimer's disease. In this context, therapeutic approaches to these disorders should necessarily incorporate strategies aimed at preserving and/or regenerating myelin.
Our research focuses on:
1. Understanding the molecular and cellular mechanisms that regulate myelin generation, maintenance, and regeneration in animal models, with a particular emphasis on oligodendroglial energy...Myelination was a key evolutionary event for the development of large and highly complex nervous systems in jawed vertebrates. Myelin, a lipid-rich membranous structure, enables the saltatory conduction of action potentials along axons and additionally provides metabolic support to axons through the supply of essential metabolites.
Loss of myelin, as well as alterations in its composition and organization can compromise axonal integrity and trigger neurodegenerative processes. Myelin abnormalities are a common feature of numerous central nervous system (CNS) pathologies, including leukodystrophies, spinal cord injuries, multiple sclerosis (MS) and other inflammatory demyelinating disorders of the CNS, periventricular leukomalacia, as well as several classical neurodegenerative diseases such as Alzheimer's disease. In this context, therapeutic approaches to these disorders should necessarily incorporate strategies aimed at preserving and/or regenerating myelin.
Our research focuses on:
1. Understanding the molecular and cellular mechanisms that regulate myelin generation, maintenance, and regeneration in animal models, with a particular emphasis on oligodendroglial energy metabolism, in order to identify novel therapeutic targets.
2. Developing therapeutic strategies aimed at stimulating myelin regeneration and maintenance in multiple sclerosis and other neurodegenerative diseases.
[Read more][Hide]
[Read more][Hide]
- Comprender los mecanismos moleculares y celulares que regulan la generación, el mantenimiento y la regeneración de la mielina en modelos animales, con especial énfasis en el metabolismo energético de las células oligodendrogliales, con el objetivo de identificar nuevas dianas terapéuticas.
- Desarrollar estrategias terapéuticas dirigidas a estimular la regeneración y el mantenimiento de la mielina en la esclerosis múltiple y otras enfermedades neurodegenerativas.
- Myelin evolution and pathologies.Myelin is a multilamellar membrane -rich structure that ensheathes the axons. We are interested in understanding how mechanisms of axo-glial communication as well as the structure and compaction of myelin evolved across different invertebrate and vertebrate species. We are also investigating myelin alterations in different models of neurodegenerative diseases
- Therapeutic strategies for myelin regeneration in neurodegenerative diseases.Myelin accelerates axonal conduction and protects axons from degeneration. We are developing potential therapeutic strategies to regenerate myelin in neurodegenerative diseases, particularly in multiple sclerosis. We are particularly interested in strategies focused on alleviating metabolic dysfunction, an important feature common to all neurodegenerative pathologies.
- Ageing and myelin dysfunction.Ageing significantly decreases the efficiency of myelin regeneration. We are studying the mechanisms underlying metabolic dysfunction of oligodendroglial cells that develops during ageing and interventions that might alleviate this dysfunction thus improve myelin regeneration and maintenance to achieve neuroprotection.
| Name | Nature of participation | Entity | Description |
|---|---|---|---|
| VANJA TEPAVCEVIC MANDIC | Director | Universitat de València | |
| Research team | |||
| LUNA MORA HUERTA | Member | Universitat de València | |
| MIGUEL FERNANDEZ POLO | Member | Universitat de València | |
| CATALINA RAVAZZANO BRAVO | Collaborator | Universitat de València | |
- -
- -
- Cavanilles Institute Biodiversity and Evolut. Biol. (ICBBE)






