Email: edith.hamel [at] mcgill.ca (Edith Hamel)
Recent Publications: PubMed
Academic Affiliations: Neurology and Neurosurgery
Research Groups: Neural Ciruits, Neurodegenerative Diseases
Dr. Edith Hamel's research focuses on the interactions between neurons, astrocytes and microvessels that assure a proper blood supply to activated brain areas, a phenomenon commonly referred to “neurovascular coupling”. These interactions are at the basis of several brain imaging techniques that use hemodynamic signals to map changes in 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 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.
Dr. Hamel uses in vivo optogenetic or electrical simulation of selected brain neurons, records the evoked neuronal and cerebral blood flow responses, identifies anatomically the neurons that are activated, and manipulates their mediators pharmacologically to define whether neurons act directly on blood vessels or indirectly through astroglial messengers. Her goal is to understand how brain neurons control local cerebral perfusion and how this relationship is altered in pathological conditions, such as in Alzheimer’s disease. The Hamel laboratory is testing the hypothesis that rescuing cerebrovascular function will have a positive outcome on the onset and progression of cognitive decline in vascular dementia and Alzheimer’s disease. Her group hypothesizes 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. Particularly, Dr Hamel’s group aims at better understanding how specific drugs can normalize cerebrovascular reactivity, brain perfusion and cognitive performance in animal models of vascular dementia or Alzheimer's disease. Additionally, she is asking whether cerebrovascular and cognitive recovery is interrelated or independent from each other. Ultimately, she and her research team aim to identify new therapeutic targets or drugs to preserve cerebral perfusion and rescue of neuronal function.
Selected Recent Publications:
(Total=148 peer-review articles):
1. Ongali B, Aboulkassim T, Tong X-K, Nicolakakis N, Rosa-Neto P, Lecrux C, Imboden H and Hamel E. (2014) Losartan rescues cerebrovascular dysfunctions and memory deficits in Alzheimer’s disease mice. Neurobiol Dis, 68: 126-136.
2. Papadopoulos P, Tong X-K, Hamel E. (2014) Selective benefits of simvastatin in bitransgenic APPSwe,Ind/TGF-b1 mice. Neurobiol Aging 35(1): 203-212.
3. Tong X-K and Hamel E. (2015) Simvastatin restored the vascular reactivity, endothelial function and reduced string vessel pathology in a mouse model of cerebrovascular disease. J Cereb Blood Flow Metab, 35(3):512-520.
4. Lacroix A, Toussay X, Anenberg E, Lecrux C, Karagiannis A, Plaisier F, Chausson P, Jarlier F, Burgess SA, Hillman EMC, Murphy TH, Hamel E and Cauli B. (2015) Prostaglandin E2 produced by pyramidal neurons underpins neurovascular coupling. J Neurosci, 35(34):11791-11810.
5. Lecrux C, Sandoe CH, Neupane S, Krop P, Toussay X, Tong X-K, Shmuel A, Hamel E. (2017). Altered brain states impact neuronal correlates of hemodynamic signals, J Neurosci, 37(6):1518-1531.
6. Badhwar A, Brown R, Stanimirovic DB, Haqqani AS, Hamel E (2017). Proteomic differences in brain vessels of Alzheimer’s disease mice: normalization by PPARγ agonist pioglitazone. J Cereb Blood Flow Metab 37 (3): 1120-1136.
7. Royea J, Zhang L, Tong X-K, Hamel E. (2017) The angiotensin IV receptor: a potential target for cerebrovascular and cognitive rescue in a mouse model of Alzheimer's disease. J Neurosci 37(32):5562-5573.