By Akio Suzumura, Kazuhiro Ikenaka
Accumulation on glia is an energetic pathological point in lots of neurological issues. Gliosis produces neuroinflammation via either neurotrophic and inflammatory capability, however the special mechanism in which this occurs stay doubtful. it truly is suspected that harm to neurons prompts the expansion of glial cells. The proposed e-book specializes in the interplay among neurons and glia to aid elucidate the pathophysiology of neuroinflammation in neurological disorders.
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Additional info for Neuron-Glia Interaction in Neuroinflammation
I. Kira T cells egress from postcapillary venules (high endothelial venules) and enter into the Virchow-Robins space (perivascular space) in the CNS. Here, activated T cells can firmly adhere to the surface of vascular endothelial cells via interactions between α4β1 integrin expressed on activated T cells and vascular cell adhesion molecule 1 (VCAM-1) on endothelial cells lining the BBB. Anti-α4β1 integrin antibody, natalizumab, effectively blocks firm adhesion of T cells, thereby markedly suppressing MS relapses (Coisne et al.
2002), which is presumably because of its consumption by infiltrating cells (Mahad et al. 2002). CCR2-deficient mice develop mild EAE with neutrophil infiltration (Yamasaki et al. 2012). Thus, macrophages play major roles in antigen presentation and tissue destruction while microglia induce tissue damage. However, microglia may also have neuroprotective properties through phagocytizing tissue debris and producing neurotrophic substances. 2 Hereditary Microgliopathy Showing Widespread Myelin and Neuroaxonal Loss Hereditary diffuse leukoencephalopathy with axonal spheroids (HDLS), a rare autosomal dominant disease characterized by cerebral white matter degeneration with axonal spheroids presenting cognitive decline, depression, and motor impairment, is caused by mutations in the CSF1R gene (Rademakers et al.
Recently, we showed the extensive loss of Cxs43, 32, and 47 in demyelinated and myelin-preserved layers of acute lesions from patients with Baló’s concentric sclerosis, a rare extremely severe variant of MS (Masaki et al. 2012). In the leading edge areas, where the expression of MAG was partly diminished with other myelin proteins well preserved, compatible with distal oligodendrogliopathy, astrocytic Cx43 was totally lost. Similar changes were also observed in MS and NMO cases culminating in death within 2 years after the disease onset (Masaki et al.