As described above, diffusion metrics including

Epacadostat molecular weight FA and ADC in the cervical spinal cord may be influenced by age-related changes. Moreover, different symptoms (e.g., paralysis and pain) show different abnormalities in diffusional metrics at each spinal cord location [5]. However, here we only compared the diffusion metrics between affected and unaffected sides and not across spinal cord levels. Therefore, longitudinal studies, a larger sample size, and clinical correlations with diffusional metrics are needed in the future to control for the influence of age-related changes and to establish diffusion metrics as clinical biomarkers. In conclusion, MK in the spinal cord may reflect microstructural changes and damage

of the spinal cord gray matter. Although further studies of the imaging–pathology relationship are needed, MK has the potential to provide new information beyond that provided by conventional diffusion metrics such as ADC and FA, which are based on the mono-exponential model. This work was supported by JSPS KAKENHI Grant Number 25461847. “
“Microglia are the resident immunocompetent and phagocytic cells in the CNS that play a critical role in normal functioning of the CNS. They respond to injury, damage and pathogens by rapidly changing their phenotype and secretion of a plethora of soluble factors. The microglia also play a key role in the communication of systemic infection and inflammation to the brain resulting Thiamine-diphosphate kinase in behavioural changes, but

this signalling is not detrimental to the adult healthy brain and rather contributes to recovery and maintenance of homeostasis (Dantzer and Kelley, MAPK Inhibitor Library purchase 2007 and Teeling and Perry, 2009). Microglia can become activated or ‘primed’ in chronic neurodegenerative or inflammatory diseases, and these primed cells, in contrast to the normal resident microglia, have a lower threshold for activation and can become harmful upon further stimulation (Cunningham et al., 2009 and Perry et al., 2010). The normal ageing process can also induce microglia priming (Chen et al., 2008, Frank et al., 2010 and Godbout et al., 2005) but the mechanism underlying these age-related changes in microglial cells are not understood. This study aimed to investigate if the age-related changes in microglia phenotype show regional differences and whether these are associated with functional changes or previously described age-related changes in neuronal integrity. Microglial cells are long lived, myeloid-derived cells that populate the CNS during early development (Alliot et al., 1999, Ginhoux et al., 2010 and Lawson et al., 1992). It is estimated that the adult mouse brain contains approximately 3.5 million microglia (Lawson et al., 1990 and Long et al., 1998). Their morphology and density, however, is region specific and can range from 5% up to 12% of total cells per region, with higher densities found in the grey matter (Lawson et al., 1990).