GENETICS OF NERVOUS SYSTEM DISEASESDifferent chromogranin immunoreactivity between prion and a-beta amyloid plaqueRangon, Claire-Marie; Haïk, StéphaneCA; Faucheux, Baptiste A.; Metz-Boutigue, Marie-Helène1; Fierville, Françoise; Fuchs, Jean-Paul1; Hauw, Jean-Jacques; Aunis, Dominique1Author Information Laboratoire de Neuropathologie Raymond Escourolle, Association Claude Bernard, INSERM Unité 360, Groupe Hospitalier Pitié-Salpêtrière, 47 Bd de l'Hôpital, 75651 Paris, Cedex 13 1INSERM Unité 338, 5 rue Blaise Pascal, 67084 Strasbourg Cedex, France CACorresponding Author Received 28 October 2002; accepted 30 October 2002 NeuroReport: April 15th, 2003 - Volume 14 - Issue 5 - p 755-758 Buy SDC Abstract Brain lesions in Creutzfeldt-Jakob disease (CJD) include spongiform change, neuronal loss, amyloid plaques, astrogliosis and microglial activation. Microglia are thought to play a key role in prion-induced neurodegeneration. However, the intermediate molecules supporting relationships between neurons and microglia are still unknown. Chromogranins (Cg) are soluble glycophosphoproteins that can activate microglial cells leading to a neurotoxic phenotype. The immunoreactive patterns of CgA and CgB were investigated in CJD and compared to those observed in Alzheimer's disease. We found that CgB, but not CgA, immunoreactivity was selectively associated with prion protein deposits, whereas CgA was only seen in Aβ plaques. This suggests a specific influence of the constitutive amyloid protein on chromogranin secretion and a role of CgB in the CJD neurodegenerative process. © 2003 Lippincott Williams & Wilkins, Inc.