Neuroinflammation, Aging and Alzheimer's Lab
Dr. Yannick Marchalant obtained his Ph.D. from the University of Caen, France in 2004. After graduating, he moved to the University of Arizona and then onto The Ohio State University as a post-doctoral researcher for 4 years. He then became a research assistant professor in 2008 at The Ohio State University for 2 years. He moved back to Europe for 4 years in Aix-Marseille University, France and joined the Psychology Department at Central Michigan University in the fall of 2014 as an assistant professor. He has been working for 15 years on neurodegenerative disease, in particular Alzheimer's disease, and has studied notably the role of neuroinflammation in brain aging as well as the influence of the endocannabinoid system on the regulation of inflammatory processes in the context of Alzheimer's disease.
I have been actively working for the past 15 years on different aspects of normal and pathological ageing (behavioural and biochemical approaches), particularly in Alzheimer's disease (AD, more precisely on the cholinergic hypothesis, neuroinflammation processes and their implication), leading to several innovative publications in the field. My work has drawn attention to the role of the endocannabinoid system in the control of neuroinflammation associated with AD.
Most recently, I have been particularly interested in:
- The effect of WIN-55, 212-2, an agonist of the GPCR endocannabinoids type 1 and 2, for its anti-inflammatory properties in a mouse model of AD (5xFAD).
- The role of the deletion of MT5-MMP in the progression of AD in 5xFAD mice.
In the few years, I would like to continue my research on the role of inflammation and its implication on learning and memory in normal and pathological aging (AD). In parallel, I want to study more closely the exact role on inflammation in the onset/progression of AD. Indeed, despite evidence in diagnosed patients and post-mortem tissues, neuroinflammation has not been definitely demonstrated as major risk factor in AD.
Marchalant Y., Brownjohn P., Bonnet A., Kleffmann T., Ashton J.:
Antibody sensitivity does not imply specificity: the cannabinoid CB2 receptor.
. J Histochemistry and Cytochemistry (2014) 62: 395-404
H.M., Bardou I., Hopp S.C.,
Marchalant Y., Kaercher R.M., Turner S.M., Mitchem M.R., Kigerl K., Wenk
Time-dependent compensatory responses to chronic neuroinflammation in hippocampus and brainstem: The potential role of glutamate neurotransmission.
J Alzheimers Dis Parkinsonism
(2013) 3: 110.
C., Roman F., Khrestchatisky
Area-specific alterations of synaptic plasticity in the 5xFAD mouse model of Alzheimer's disease: Dissociation between somatosensory cortex and hippocampus
(2013) 8: e74667.
Bardou I., DiPatrizio N., Brothers
H.M., Kaercher R.M., Baranger
K., Mitchem M., Hopp S.C., Wenk
Pharmacological manipulation of cannabinoid neurotransmission reduces neuroinflammation associated with normal aging.
(2012) 4: 679-84.
Marchalant Y., Baranger K., Wenk G.L., Khrestchatisky M., Rivera S.: Can the benefits of cannabinoid receptor stimulation on neuroinflammation, neurogenesis and memory during normal aging be useful in AD prevention?
J Neuroinflammation. (2012) 9:10.
Marchalant Y., Wenk G.L.: Caffeine attenuates lipopolysaccharide-induced neuroinflammation.
Neurosci Lett. (2010) 480:97-100
Brothers H.M., Wenk G.L.: Cannabinoid Agonist win-55,212-2 partially restores neurogenesis in the aged rat brain.
Molecular psychiatry, (2009) 14: 1068-1071
Brothers H.M., Norman G.H., Karelina K., Devries A.C., Wenk G.L.: Cannabinoids attenuate the effects of aging upon neuroinflammation and neurogenesis.
Neurobiol. Dis. (2009) 34(2): 300-307