Enhanced expression of 14-3-3 proteins in reactive astrocytes in Creutzfeldt-Jakob disease brains

• Published in: Acta Neuropathologica Vol. 108; no. 4; pp. 302 - 308
• Main Authors: Kawamoto, Yasuhiro, Akiguchi, Ichiro, Jarius, Christa, Budka, Herbert
• Format: Journal Article
• Language: English
• Published: Germany Springer Science and Business Media LLC 01.10.2004; Springer Nature B.V
• Subjects: 14-3-3 Proteins; 14-3-3 Proteins - biosynthesis; Aged; Alzheimer Disease; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Astrocytes; Astrocytes - metabolism; Astrocytes - pathology; Brain; Brain - metabolism; Brain - pathology; Creutzfeldt-Jakob Syndrome; Creutzfeldt-Jakob Syndrome - metabolism; Creutzfeldt-Jakob Syndrome - pathology; Female; Humans; Immunohistochemistry; Male; Middle Aged; Neurofibrillary Tangles; Neurofibrillary Tangles - metabolism; Neurofibrillary Tangles - pathology; Neurons; Neurons - metabolism; Neurons - pathology
• ISSN: 0001-6322; 1432-0533
• DOI: 10.1007/s00401-004-0892-5

14-3-3 proteins have been reported to be detected specifically in the cerebrospinal fluid (CSF) from patients with Creutzfeldt-Jakob disease (CJD). To elucidate the role of 14-3-3 proteins in patients with CJD, we performed immunohistochemical studies on 14-3-3 proteins in autopsied brains from five patients with sporadic CJD (sCJD), three patients with Alzheimer's disease (AD), and seven normal control subjects. Formalin-fixed, paraffin-embedded sections from all cases were immunostained with several types of specific anti-14-3-3 antibodies. In the normal control brains, 14-3-3 immunoreactivity was localized mainly in the neuronal somata and processes; in contrast, glial cells showed no or faint immunoreactivity. In the brains from the patients with AD, 14-3-3 immunoreactivity was observed in the surviving neurons as well as some neurofibrillary tangles. In the brains from the patients with sCJD, 14-3-3 immunoreactivity was well preserved in the remaining neurons. Furthermore, the glial cells, especially the reactive astrocytes, were intensely immunostained in the brains affected by sCJD. Our findings suggest that 14-3-3 proteins may be up-regulated in the glial cells, particularly in reactive astrocytes, and that the enhanced expression of 14-3-3 proteins in these glial elements may be associated with the pathogenesis of sCJD.