Dr. Edith Hamel's research focusses on the interactions that take place between neurons, astrocytes and microvessels to assure a proper blood supply to activated brain areas, a phenomenon commonly referred to “neurovascular coupling”. These interactions are at the basis of the signals used in brain imaging studies to map brain activity under physiological and pathological conditions. The underlying cellular mechanisms and chemical mediators of these signals are poorly understood. This is important because the dysfunction/degeneration of specific populations of cells might have dramatic repercussions on the regulation of local blood flow. Moreover, several neurological conditions are associated with a cerebrovascular pathology and impaired neurovascular coupling responses. One such condition is Alzheimer's disease, in which the cerebrovascular dysfunction is an integral part of the disease process. Dr. Hamel uses in vivo simulation of selected brain pathways, records the evoked cerebral blood flow response, identifies anatomically the neurons that are activated in line with the perfusion response, and manipulates their mediators pharmacologically to define whether neurons act directly on blood vessels or indirectly through astroglial messengers. She also characterizes the receptors involved. Her goal is to understand how brain neurons control local cerebral perfusion and how this relationship is altered in pathological conditions. An active part of the laboratory is concerned with the neuronal and cerebrovascular pathologies in Alzheimer's disease, particularly how specific drugs can normalize cerebrovascular reactivity, brain perfusion and cognitive performances in animal models of Alzheimer's disease. Her laboratory is testing the hypothesis that rescuing cerebrovascular function will have a positive outcome on disease progression, and that it might be possible, at specific time points in the disease, to rescue or delay the manifestation of cognitive alterations by improving brain perfusion. Additionally, her laboratory is asking whether it is possible to pharmacologically rescue both cerebrovascular and memory deficits in Alzheimer mouse models, and if their recovery is interrelated or independent from each other. Dr. Hamel investigates the mechanisms that underlie their respective recovery. Ultimately, she and her research team aim to identify new therapeutic targets or drugs to preserve cerebral perfusion together with or independently from rescue of neuronal function.

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E-mail: Edith Hamel