Stress protein expression in the Alzheimer-diseased choroid plexus

Article type: Research Article

Authors: Anthony, Shawn G.^a | Schipper, Hyman M.^b | Tavares, Rosemarie^a | Hovanesian, Virginia^a | Cortez, Selina C.^a | Stopa, Edward G.^a | Johanson, Conrad E.^{c; *}

Affiliations: [a] Division of Neuropathology, Department of Pathology, Rhode Island Hospital, Brown Medical School, Providence, RI 02903, USA | [b] Centre for Neurotranslational Research, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, H3T 1E2 Canada | [c] Department of Clinical Neurosciences (Neurosurgery) Rhode Island Hospital, Brown Medical School, Providence, RI 02903, USA

Correspondence: [*] Corresponding author. Conrad E. Johanson, Ph.D., Department of Neurosurgery, Rhode Island Hospital, 593 Eddy Street (Aldrich 401), Providence, RI 02903, USA. Tel.: +1 401 444 8739; Fax: +1 401 444 8727; E-mail: [email protected].

Abstract: Abnormal patterns of stress protein expression are found in the cerebral cortex and hippocampus of Alzheimer (AD) subjects. In this study, expression of various stress proteins in the Alzheimer-diseased choroid plexus (CP) was assessed immunohistochemically. We observed decreased HO-1 immunoreactivity in the AD CP, commensurate with our earlier report of suppressed HO-1 protein levels in AD cerebrospinal fluid (Schipper et al., Neurology 54:1297–1304, 2000). Heat shock protein (HSP) 90 was up-regulated in the AD CP relative to controls. There was a trend towards increased expression of HSP60, a mitochondrial stress protein; this is compatible with mitochondrial pathology recently documented in AD CP. Up-regulation of HSP90, a steroid receptor chaperone, in the AD CP may indicate abnormal hormone receptor expression in this secretory tissue. Glucose-regulated protein (GRP) 78 and 94 immunostaining was diminished in AD CP, implicating possible derangements in glucose or calcium homeostasis. Oxidative stress, per se, is probably not responsible for our observations because: i) there were no noticeable differences in the expression of HSP 70, ubiquitin, and alpha-B crystallin in the AD CP; and ii) augmentation, rather than the noted suppression, of HO-1 immunoreactivity would have been expected.

Keywords: Alzheimer's disease, choroid plexus, alpha-B crystallin, heat shock protein, oxidative stress, heme oxygenase-1, ubiquitin

DOI: 10.3233/JAD-2003-5301

Journal: Journal of Alzheimer's Disease, vol. 5, no. 3, pp. 171-177, 2003