Astrocytic expression of adiponectin receptor 2 in the 5XFAD mouse model of Alzheimer’s disease
Anishchal Pratap (1, 2) and R. M. Damian Holsinger (1, 2)
Laboratory of Molecular Neuroscience and Dementia, Brain and Mind Centre, School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, New South Wales, Australia
Discipline of Pathology, School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, New South Wales, Australia
Alzheimer’s disease (AD) is an age-related neurodegenerative disease afflicting over 35 million sufferers worldwide. The condition generally affects ~5% of the population over the age of 65, with the incidence doubling every 5 years thereafter. The pathological origins of AD are currently unknown and therefore treatment only addresses early symptomatic issues. Metabolic syndromes such as diabetes and obesity are strongly correlated with AD, with common pathologies including cortical atrophy, insulin resistance and inflammation. Adiponectin, a cytokine secreted by adipose tissue modulates metabolism and energy distribution via its receptors, AdipoR1 and AdipoR2. To determine whether adiponectin receptors play a role in energy metabolism in the AD brain, we assessed their expression in the brains of the 5XFAD mouse model of AD. Mice were sacrificed at different stages of disease progression and expression of AdipoR1, AdipoR2 and the astrocyte marker GFAP was examined by immunofluorescence staining. Results show increased expression of GFAP in old compared to young 5XFAD mice. While AdipoR1 and AdipoR2 were expressed throughout the brain in aged mice, AdipoR1 expression was localized to endothelial cells while AdipoR2 was strongly expressed in astrocytes. Increased astrocytic and decreased neural expression of AdipoR2 as the AD mice age supports metabolic disturbance as a concomitant feature of AD.