ELSEVIER Neuroscience Letters 213 (1996) 189-192 NEUROSCiENC[ IETT[IlS Increased tau immunoreactivity in oligodendrocytes following human stroke and head injury E.A. Irving a'*, J. Nicoll b, D.I. Graham b, D. Dewar a ~Wellcome Surgical Institute and Hugh Fraser Neurascience Laboratories, Garscube Estate, Bearsden Road, Glasgow, G61 1QH, UK bDepartment of Neuropathology, University of Glasgow, Glasgow, UK Received 18 April 1996; revised version received 27 June 1996; accepted 27 June 1996 Abstract Tau immunohistochemistry was performed on post-mortem brain tissue from patients who died following head injury or stroke and from neurologically norm~Ll controls. Tau-positive oligodendrocytes were detected with three different tau antibodies in head injured or stroke patients, but not i~a control cases. Tau-positive oligodendrocytes were detected 2 h following head injury indicating that accumulation of tau may be an acute response of these cells to brain injury. The mechanisms underlying accumulation of tau in oligodendrocytes after acute brain injury may be similar to those which occur in chronic neurodegenerative conditions such as progressive supranuclear palsy (PSP) and multi-system atrophy (MSA). Keywords: Tau; Cytoskeleton; Oligodendrocyte; Stroke; Head injury Accumulation of the microtubule associated protein (MAP) tau within neuronal perikarya and the subsequent formation of neurofibrillary tangles is thought to be central to neuronal degeneration in Alzheimer's disease. How- ever, disruption of the neuronal cytoskeleton may repre- sent a final common pathway of degeneration in a variety of both chronic and acute neurodegenerative conditions. In experimentally-induced acute brain injury resulting from cerebral ischaemia or excessive glutamate receptor stimu- lation, changes in neuronal tau immunostaining have been reported [7,8,10]. However, in addition to changes in neu- ronal tau, we have previously reported increased immu- noreactivity of this protein in glial cells following either focal cerebral ischaemia or in response to high concentra- tions of glutamate in vivo [7,9,10]. In both experimental models, tau-positive glial cells were present within a few hours of induction of the neuronal insult and the cells have been confirmed as oligodendrocytes [9, I0]. It is crucial to gain an understanding of the role that these cells may play in the pathology of both chronic and acute neurodegenera- tive diseases. Tau-positive glial inclusions are a prominent * Corresponding author. Tel.: +44 141 3305829; fax: +44 141 9430215; e-mail: 932954ir @ udcf.gla.ac.uk feature in post-mortem brain in various slowly progressing degenerative conditions including multi-system atrophy (MSA) and progressive supranuclear palsy (PSP) [1,11, 12,14,16]. It is possible to speculate that there may be similar mechanisms underlying the accumulation of tau in oligodendrocytes in both acute and chronic neurodegen- erative conditions. In order to investigate this we have examined tau immunostaining in post-mortem brain tissue of patients dying following head injury or stroke and nor- mal control cases. The accumulation of tau in oligoden- drocytes as early as 2 h following head injury suggests that this is an early response of these cells to injury. Formalin-fixed paraffin-embedded post-mortem brain tissue from 11 patients dying following head injury and four patients dying following cerebral ischaemia was used in this study (Table 1). Seven cases with no previous neu- rological conditions served as controls (Table 2). The cor- pus callosum of head injury patients was examined as this area is most susceptible to diffuse axonal injury related to head injury [2] and in stroke patients areas of infarcted tissue were examined. Tau was detected using three dif- ferent antibodies, Tau 1 [3,15], TP007 [6] and TP70 [4]. Immunolabeling was detected using the avidin-biotin complex method (ABC kit, Vector) and visualised by 3'- 0304-3940/96/$12.00 © 1996 Elsevier Science Ireland Ltd. All rights reserved PII S0304-3940(96) 12856- 1