(Stroke. 1995;26:2145-2148.)
© 1995 American Heart Association, Inc.
Articles |
From the Department of Neuropathology, Tokyo Institute of Psychiatry (T.U., H.K., K.I.); Department of Neurology, Tokyo Medical and Dental University (T.U., K.T.); Department of Pathology, Tokyo Medical College (K.T.); and Department of Pathology, Tokyo Metropolitan Aoyama Hospital (T.H.) (Japan).
Correspondence to T. Uchihara, MD, PhD, Laboratoire Raymond Escourolle, Service de Neuropathologie, Groupe hospitalier, Pitié-Salpêtrière, 47-83 Boulevard de l'Hôpital, 75651 Paris, Cedex 13, France.
Background and Purpose Tau-like immunoreactivity is known to develop in neurons under some experimental conditions simulating ischemia. The purpose of this study is to investigate the expression of tau-like immunoreactivity in the human brain after ischemic insult.
Methods A series of autopsied human brains with or without ischemic lesion were investigated with immunohistochemistry (Alz-50, anti-tau, and anti-ubiquitin) and with silver-staining methods (Gallyas and Bodian methods).
Results Punctate immunoreactivity to Alz-50 was visualized in the cytoplasm not only of the neurons in and around the ischemic lesion but also of the neurons free from classic ischemic changes around the necrosis. Some of the neurons around the ischemic lesion were stained by the Gallyas method. Immunostaining with anti-tau and anti-ubiquitin antibodies and the conventional Bodian method failed to visualize these neurons.
Conclusions The widespread appearance of Alz-50 immunoreactive neurons during the ischemic process signifies that tau-related proteins may be related to ischemic necrosis, but the lack of neurofibrillary tangles morphologically distinguishes ischemic development of tau-related proteins from the neurofibrillary degeneration in Alzheimer's disease.
Key Words: cerebral infarction neurofibrillary tangles tau proteins
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