Increased Selenoprotein P in Choroid Plexus and Cerebrospinal Fluid in Alzheimer's Disease Brain

Article type: Short Communication

Authors: Rueli, Rachel H.L.H.^a | Parubrub, Arlene C.^a | Dewing, Andrea S.T.^a | Hashimoto, Ann C.^a | Bellinger, Miyoko T.^a | Weeber, Edwin J.^b | Uyehara-Lock, Jane H.^c | White, Lon R.^d | Berry, Marla J.^a | Bellinger, Frederick P.^{a; *}

Affiliations: [a] Cell and Molecular Biology Department, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA | [b] Molecular Pharmacology and Physiology, University of South Florida, Johnnie B. Byrd, Sr. Alzheimer's Center & Research Institute, Tampa, FL, USA | [c] Pathology Department, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA | [d] Pacific Health Research and Education Institute, Honolulu, HI, USA

Correspondence: [*] Correspondence to: Frederick P. Bellinger, Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii, 651 Ilalo St, Honolulu, HI 96813, USA. Tel.: +1 808 692 1512; Fax: +1 808 692 1970; E-mail: fb@hawaii.edu.

Abstract: Subjects with Alzheimer's disease (AD) have elevated brain levels of the selenium transporter selenoprotein P (Sepp1). We investigated if this elevation results from increased release of Sepp1 from the choroid plexus (CP). Sepp1 is significantly increased in CP from AD brains in comparison to non-AD brains. Sepp1 localizes to the trans-Golgi network within CP epithelia, where it is processed for secretion. The cerebrospinal fluid from AD subjects also contains increased levels Sepp1 in comparison to non-AD subjects. These findings suggest that AD pathology induces increased levels of Sepp1 within CP epithelia for release into the cerebrospinal fluid to ultimately increase brain selenium.

Keywords: Alzheimer's disease, cerebrospinal fluid, choroid plexus, selenium, selenoprotein P, selenoproteins, Sepp1

DOI: 10.3233/JAD-141755

Journal: Journal of Alzheimer's Disease, vol. 44, no. 2, pp. 379-383, 2015