“
“M. Ndung’u, W. Härtig, F. Wegner, J. M. Mwenda, R. W. C. Low, R. O. Akinyemi and R. N. Kalaria (2012) Neuropathology and Applied Neurobiology38, 487–499 Cerebral amyloid β(42) deposits and microvascular Selleckchem MI-503 pathology in

ageing baboons Background: Previous studies have extensively reported the deposition of amyloid β (Aβ) peptide with carboxyl- and amino-terminal heterogeneity in cortical and cerebrovascular deposits in Alzheimer’s disease (AD) and in non-human primates except baboons. Methods: We examined the immunocytochemical distribution of Aβ peptides and Aβ oligomers in brain tissue from three subspecies of 18- to 28-year-old baboons (Papio) and in other monkeys including the squirrel (Saimiri sciureus) and rhesus (Macaca mulatta) for comparison. Results: A general preponderance of Aβ(42) in parenchymal deposits and many vascular deposits in all cortical lobes was evident in the baboons. Aβ oligomeric immunoreactivity was also apparent like to amyloid plaques. We found that the amino acid sequence of the Aβ domain of the baboon amyloid precursor

protein is similar to that of man. In contrast to Aβ, immunoreactivity to hyperphosphorylated tau protein was largely intracellular and rare in these baboons. Brain tissues from squirrel and rhesus monkeys examined in parallel exhibited mostly vascular see more and parenchymal deposits containing Aβ(42) peptides. Our results were comparable to AD, but showed Urocanase that even in younger monkeys exhibiting few deposits, Aβ(42) was evident in both parenchymal deposits and cerebral amyloid angiopathy. Perivascular amyloid deposits were frequent and often accompanied by microvascular abnormalities in the form of collapsed degenerated capillaries. Conclusions: Similar to other primates above and below in the phylogenetic order, our observations and evaluation of

the literature implicate pathogenicity of Aβ(42) peptide associated with microvascular degeneration in baboons. We suggest baboons are useful animals to investigate the dynamics of AD-related pathology. “
“Neuromyelitis optica (NMO) is an inflammatory demyelinating and necrotizing disorder of the CNS that mainly affects the optic nerve and spinal cord. The etiology is still uncertain; however, the discovery of serum anti-aquaporin-4 (AQP4) autoantibody is becoming the center of attention, and a new hypothesis is emerging that NMO is essentially astrocytopathy provoked by this autoantibody. In this study, we focused on corpora amylacea (CA), glycoproteinaceous inclusions in astrocytic processes. We examined 57 lesions in nine cases of NMO spectrum disorder, and demonstrated that CA were phagocytized by macrophages in 42 lesions (74%) of eight cases, while phagocytized figures were not seen in unaffected areas. Phagocytized CA were frequently encountered in early-phase lesions still retaining myelin structures, while fewer or none were found in chronic destructive lesions.