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Microglia-neuron communication and neurodegeneration in multiple sclerosis
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Dr. Cardona studies inflammatory processes in the central nervous system (brain, spinal cord, and retina), focusing on autoimmune diseases, particularly multiple sclerosis and diabetes-associated vision loss (retinopathy). Autoimmune diseases are complex disorders with underlying mechanisms characterized by immune responses against self. The incidence of autoimmune diseases has tripled in the past decades, and with the obesity epidemic, the incidence of blindness due to diabetes is expected to escalate. The overarching goal of her research is to elucidate potential anti-inflammatory pathways for clinical intervention in autoimmune diseases.
Mechanism of communication between neurons and resident tissue macrophages (microglia) is her primary focus. Her research focuses on the interaction between the neuronal fractalkine (FKN) and its microglial receptor CX3CR1. Microglia are essential cells that support the function of neurons. Microglial cells are sensors of injury, constantly searching for damage, injured or unnecessary neurons, synapses, and infectious agents. However, exaggerated responses of microglia in response to injury can lead to bystander damage to neurons. Her studies have shown that both FKN and CX3CR1 are highly abundant in the brain, spinal cord, and retina and directly inhibit microglia’s inflammatory behavior. In humans, mutations in the CX3CR1 gene give rise to a defective receptor in its ability to bind the FKN. Therefore, understanding the role of the human versions of CX3CR1 is of clinical relevance for targeted clinical approaches. To address this, her team has developed an experimental model to study the human polymorphic variant and how the expression of these altered receptors affects disease initiation and progression. Her interest in elucidating the role of environmental factors (metabolic endotoxemia and recurrent infections) in disease susceptibility will be instrumental in understanding neuronal-microglia communication to regulate immune-mediated damage and facilitate tissue repair.
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