Aβ1–42 stimulated T cells express P-PKC-δ and P-PKC-ζ in Alzheimer disease

• Published in: Neurobiology of aging Vol. 30; no. 3; pp. 394 - 406
• Main Authors: Miscia, Sebastiano, Ciccocioppo, Fausta, Lanuti, Paola, Velluto, Lucia, Bascelli, Adriana, Pierdomenico, Laura, Genovesi, Domenico, Di Siena, Alessandro, Santavenere, Eugenio, Gambi, Francesco, Ausili-Cèfaro, Giampiero, Grimley, Philip M, Marchisio, Marco, Gambi, Domenico
• Format: Journal Article
• Language: English
• Published: London Elsevier 01.03.2009
• Subjects: Biological and medical sciences; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Development. Senescence. Regeneration. Transplantation; Fundamental and applied biological sciences. Psychology; Internal Medicine; Medical sciences; Neurology; Vertebrates: nervous system and sense organs; Flow cytometry; Protein kinase C; Alzheimer's disease; T-cell activation; Nervous system diseases; Senescence; Enzyme; Alzheimer disease; Transferases; Cerebral disorder; Central nervous system disease; T-Lymphocyte; Degenerative disease
• ISSN: 0197-4580; 1558-1497
• DOI: 10.1016/j.neurobiolaging.2007.07.011

Abstract The protein kinase C (PKC) family of enzymes is a regulator of transmembrane signal transduction, and involvement of some PKC isoforms in T-cell activation has been demonstrated. Nevertheless, very little is known about their involvement in the Amyloid β (Aβ)-dependent molecular signals in the T lymphocytes of Alzheimer disease (AD) patients. Therefore, the aim of this study was to investigate the involvement of PKC-α, PKC-δ and PKC-ζ expression and activity in the signaling machinery activated in Aβ-reactive T cells, in adult healthy individuals, elderly healthy subjects, and from patients with AD. The results show that in peripheral T-cells from early AD patients, Aβ1–42 produced a distinct subpopulation highly expressing P-PKC-δ, while in severe AD patients the same treatment induced two distinct P-PKC-δ and P-PKC-ζ T-cell subpopulations. Such subpopulations were not noticeable following CD3/CD28 treatment of the same samples or after treatment of peripheral T cells from healthy adult or elderly subjects with Aβ1–42 or with CD3/CD28. We believe that these findings may be of help in possible attempts to develop further diagnostic strategies useful for the characterization of AD.