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5TH INTERNATIONAL CONFERENCE ON METALLOTHIONEIN SYMPOSIUM PAPERS

Expression of Metallothionein-I, -II, and -III in Alzheimer Disease and Animal Models of Neuroinflammation

Juan Hidalgo^*,1, Milena Penkowa, Carmen Espejo, Eva M. Martínez-Cáceres, Javier Carrasco^*, Albert Quintana^*, Amalia Molinero^*, Sergi Florit^*, Mercedes Giralt^* and Arantxa Ortega-Aznar^||

^* Institute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Animal Physiology Unit, Faculty of Sciences, Autonomous University of Barcelona, Bellaterra, Barcelona, Spain 08193; Department of Medical Anatomy, The Panum Institute, University of Copenhagen, Copenhagen, Denmark; Unitat de Neuroimmunologia Clínica, Institut de Recerca-Hospital Universitari Vall d’Hebron, Barcelona, Spain; Laboratory of Immunology for Research Applied to Diagnosis (LIRAD)–Tissue and Blood Bank (BST), Institut d’investigació en Ciències de la Salut Germans Trias i Pujol, Badalona, Barcelona, Spain; and ^|| Neuropathology Unit, Department of Pathology, Vall d’Hebron Universitary Hospital. Barcelona, Spain

To whom requests for reprints should be addressed at ¹ Institute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Animal Physiology Unit, Faculty of Sciences, Autonomous University of Barcelona, Bellaterra, Barcelona, Spain 08193. E-mail: Juan.Hidalgo{at}uab.es

Abstract

In recent years it has become increasingly clear that the metallothionein (MT) family of proteins is important in neurobiology. MT-I and MT-II are normally dramatically up-regulated by neuroinflammation. Results for MT-III are less clear. MTs could also be relevant in human neuropathology. In Alzheimer disease (AD), a major neurodegenerative disease, clear signs of inflammation and oxidative stress were detected associated with amyloid plaques. Furthermore, the number of cells expressing apoptotic markers was also significantly increased in these plaques. As expected, MT-I and MT-II immunostaining was dramatically increased in cells surrounding the plaques, consistent with astrocytosis and microgliosis, as well as the increased oxidative stress elicited by the amyloid deposits. MT-III, in contrast, remained essentially unaltered, which agrees with some but not all studies, of AD. In situ hybridization results in a transgenic mouse model of AD amyloid deposits, the Tg2576 mouse, which expresses human Aß precursor protein harboring the Swedish K670N/M671L mutations, are in accordance with results in human brains. Overall, these and other studies strongly suggest specific roles for MT-I, MT-II, and MT-III in brain physiology.

Key Words: metallothionein-I • metallothionein-II • metallothionein-III • Alzheimer disease • transgenic mice • Tg2576 • neuroinflammation