Intermittent cytomegalovirus infection alters neurobiological metabolism and induces cognitive deficits in mice.

Risk factors contributing to dementia are multifactorial. Accumulating evidence suggests a role for pathogens as risk factors, but data is largely correlative with few causal relationships. Here, we demonstrate that intermittent murine cytomegalovirus (MCMV) infection of mice, alters blood brain barrier (BBB) permeability and metabolic pathways. Increased basal mitochondrial function is observed in brain microvessels cells (BMV) exposed to intermittent MCMV infection and is accompanied by elevated levels of superoxide. Further, mice score lower in cognitive assays compared to age-matched controls who were never administered MCMV. Our data show that repeated systemic infection with MCMV, increases markers of neuroinflammation, alters mitochondrial function, increases markers of oxidative stress and impacts cognition. Together, this suggests that viral burden may be a risk factor for dementia. These observations provide possible mechanistic insights through which pathogens may contribute to the progression or exacerbation of dementia.

Monitoring ADSC Metabolism Using the Seahorse Analyzer.

Bioenergetic and biosynthetic processes are key indicators regulating adipose-derived stromal/stem cell (ADSC) function, health, and differentiation. A common method used to metabolically profile cells is the Seahorse XF Analyzer. This live-cell assay can be used to define key metabolic pathways, including glycolysis and oxidative phosphorylation. Here, we share optimized protocols to characterize metabolism of ADSCs under basal conditions and provide insight into further assays defining metabolic changes and/or dependency during ADSC differentiation.