Plaques, neuritic, in Alzheimer’s disease

Benveniste, H. Einstein, G. Kim, K. R. et al. Detection of neuritic plaques in Alzheimer s disease by magnetic resonance microscopy. 

Xia M, Qin S, McNamara M, Mackay C, Hyman BT (1997) lnterleukin-8 receptor B immunore-activity in brain and neuritic plaques of Alzheimer s disease. Am J Pathol 150 1267-1274 Xia MQ, Bacskai BJ, Knowles RB, Qin SX, Hyman BT (2000) Expression of the chemokine receptor CXCR3 on neurons and the elevated expression of its ligand IP-10 in reactive astrocytes in vitro ERKl/2 activation and role in Alzheimer s disease. J Neuroimmunol 108 227-235 Xia MQ, Qin SX, Wu LJ, Mackay CR, Hyman BT (1998) Immunohistochemical study of the beta-chemokine receptors CCR3 and CCR5 and their Ugands in normal and Alzheimer s disease brains. Am J Pathol 153 31-37... 

Xia M, Qin S, McNamara M, Mackay C, Hyman B (1997) Interleu-kin-8 receptor B immunoreactivity in brain and neuritic plaques of Alzheimer s disease. Am J Pathol 150 1267-1274. 

Landsberg, J.P., McDonald, B. and Watt, F. (1992). Absence of aluminium in neuritic plaque cores in Alzheimer s disease. Nature 360, 65-68. 

Neuritic (senile) plaques Microscopic lesions composed of fragmented axon terminals and dendrites surrounding a core of amyloid seen in the cerebral cortex in Alzheimer s disease. 

Neuroanatomical and neuropathological basis of Alzheimer s disease Histological features of Alzheimer s disease include neuritic plaques and neurofibrillary tangles (Boiler and Duyckaerts 1997). Neuritic plaques are composed of extracellular deposits of j8-amyloid protein and apolipoprotein E and are found primarily in neocortex. j8-amyloid is derived from an amyloid precursor protein, and is suspected to be a chief causal factor in Alzheimer s disease pathology (Samuel et al. 1997). Neurofibrillary tangles are clusters of protein fibers found in the cell body and composed of tau protein, which normally serves as a cytoskeletal element. Neurofibrillary tangles progress from entorhinal cortex to hippocampus, and then to neocortical areas. 

Praprotnik D, Smith MA, Richey PL, Vinters H V, Perry G (1996) Filament heterogeneity within the dystrophic neurites of senile plaques suggests blockage of fast axonal transport in Alzheimer s disease. Acta Neuropathol (Berl) 91 226-235... 

Sheng J, Griffin W, Royston M, Mrak R (1998) Distribution of interleukin-1-immunoreactive microglia in cerebral cortical layers Implications for neuritic plaque formation in Alzheimer s disease. Neuropathol Appl Neurobiol 24 278-283. 

Hull M, Berger M, Volk B, Bauer 1 (1996) Occurrence of interleukin-6 in cortical plaques of Alzheimer s disease patients may precede transformation of diffuse into neuritic plaques. Ann N Y Acad Sci 777 205-212. 

Benito C, Nunez E, Tolon RM, Carrier EJ, Rabano A, Hillard CJ, Romero J (2003) Cannabinoid CB2 receptors and fatty acid amide hydrolase are selectively overexpressed in neuritic plaque-associated glia in Alzheimer s disease brains. J Neurosci 23 11136-11141... 

Arcndt, T. BigI, V., Tenn-stedt, A., and Arendt, A. (1985). Neuronal los.s in different parts of the nucleus basalLs is related to neuritic plaque formation in cortical target areas in Alzheimer s disease. Neuroscience 14,1-14. 

Other previous studies have also demonstrated the presence of CB2 expression in the rat microglial cells (7), in cerebral granule cells (8,11), and in mast cells 9). Furthermore, new research indicates that CB2 receptors are expressed by a limited population of microglial cells in normal healthy and in neuritic plaque-associated glia in Alzheimer s disease brain (10-13). 

Montine, TJ, Markesbery, WR, Zackert, W, Sanchez, SC, Roberts, LJ, It and Morrow, JD (1999c) The magnitude of brain lipid peroxidation correlates with the extent of degeneration but not with the density of the neuritic plaques and neorofibrillary tangles or with APOE genotype in Alzheimer s disease patients. Am J Pathol, 155, 863-868. 

Finally, it should be noted that not only are KSPGs present in the normal brain, associated with most neurons of the cerebral cortex, for example, but also that the epitope for highly sulfated KS chains disappears from these neurons in Alzheimer s disease [55]. However, the periphery of Alzheimer s disease neuritic plaques is positive for KS [56]. 

Figure 18.1 Typical tangle (T) and plaque (P) as visualised by silver impregnation in the cerebral cortex of a case of Alzheimer s disease. The extracellular plaque (10-50 pm diameter) consists of a central core of amyloid surrounded by glial processes and a number of neurites in a ring formation. The intracellular cytoplasmic tangle is composed of helical filaments in a paired format. (Reproduced with permission of Academic Press from Wischik and Crowther 1986)...

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