Carlos Camara-Lemarroy

Assistant Professor

Clinical Neurosciences

Full Member

Hotchkiss Brain Institute

M.D. (Doctor of Medicine)


Contact information

Location

Office : HMRB190

Preferred method of communication

Administrative Assistant:
Bev Clair
P: 403.210.6560
E: bclair@ucalgary.ca

 


Research and teaching

Research areas

  • Multiple Sclerosis
  • Neuroimmunology
  • MS

Research activities

Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system (CNS) characterized by the presence of multifocal lesions with demyelination and axonal injury. A vast number of studies have demonstrated a remarkable role for the gut microenvironment, gut microbiota and their metabolites in influencing peripheral immune cell function and in regulating immune responses and neuroinflammatory processes in the. This gut-brain axis acts as a bidirectional link that allows communication between the brain and the gut. There is accumulating evidence suggesting that the gut-brain axis plays an important role in the pathophysiology of MS. However, most research has focused on the microbiome, the abundant and complex population of microbial commensals inhabiting the intestinal tract, while the role of intestinal barrier and its dysfunction has lacked attention. My research focuses on the factors involved in disrupting the intestinal barrier in response to inflammatory and microbiome signals, and how these factors may affect blood brain barrier permeability and neuroinflammation. This could help explain how the gut-brain axis relates to MS pathophysiology and lead to new treatment approaches.

In MS, the CNS lesion microenvironment undergoes various alterations that impair remyelination. There is also an unmet need for a clinically effective and safe intervention to promote remyelination and repair in MS. Another research interest of mine is the potential of remote ischemic preconditioning (an intervention with known neuroprotective and immune modulating properties) to improve remyelination, and to elucidate possible mechanisms involved, in order to provide a translational framework for REIP-induced repair to benefit those living with MS.


Publications

PubMed