BS, Biological Sciences
University of Salamanca
MSc, Vision Sciences
University of Valladolid
IOBA, University of Valladolid, Spain
Pedram Hamrah, MD, Adviser
With almost 30% of the population affected, dry eye disease (DED) is an ocular surface disorder showing instability of the tear film, inflammation, nerve degeneration and comorbid pain. The instability of the tear film increases tear osmolality and consequently results in desiccation, which induces epithelial injury with transient nerve degeneration, release of pro-inflammatory mediators, subsequent chronic corneal inflammation and often corneal neuralgia. The neuropathic pain is originated by central sensitization as the result of the ongoing damage to peripheral sensory neurons and by focally released pro-inflammatory mediators. The chronic release of inflammatory molecules results in modified ion channels distribution and altered neuronal properties that modulate the excitability of nociceptor terminals. The damage of the corneal nerves and the altered immune profile also provoke changes in the vascular system of the ocular surface. My research focuses in investigate the underlying crosstalk between nervous, immune and vascular systems in the ocular surface and search for new therapeutic approaches to treat neuropathic pain.
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