NEUROFIBRILLARY LESIONS IN EXPERIMENTAL ALUMINUM-INDUCED ENCEPHALOPATHY AND ALZHEIMERS-DISEASE SHARE IMMUNOREACTIVITY FOR AMYLOID PRECURSORPROTEIN, A-BETA, ALPHA(1)-ANTICHYMOTRYPSIN AND UBIQUITIN-PROTEIN CONJUGATES

Citation
Y. Huang et al., NEUROFIBRILLARY LESIONS IN EXPERIMENTAL ALUMINUM-INDUCED ENCEPHALOPATHY AND ALZHEIMERS-DISEASE SHARE IMMUNOREACTIVITY FOR AMYLOID PRECURSORPROTEIN, A-BETA, ALPHA(1)-ANTICHYMOTRYPSIN AND UBIQUITIN-PROTEIN CONJUGATES, Brain research, 771(2), 1997, pp. 213-220
Citations number
44
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
771
Issue
2
Year of publication
1997
Pages
213 - 220
Database
ISI
SICI code
0006-8993(1997)771:2<213:NLIEAE>2.0.ZU;2-L
Abstract
Neurofibrillary tangles of Alzheimer's disease contain predominantly t au protein and to a lesser de ee amyloid precursor protein (APP), A be ta protein, alpha(1)-antichymotrypsin (ACT) and ubiquitin. Previously we have demonstrated the presence of phosphorylated tau and neurofilam ent proteins in neurofibrillary degeneration (NFD) induced by aluminum (Al) maltolate in rabbits [Savory et al., Brain Res. 669 (1995) 325-3 29; Savory et al., Brain Res. 707 (1996) 272-281]. Using the same anim al system we have now detected APP, A beta, ACT and ubiquitin-like imm unoreactivities in NFD-bearing neurons, often colocalizing in the NFD. Diffuse cytoplasmic staining for APP, A beta and ubiquitin was also p resent in neurons without NFD from Al maltolate-treated rabbits. This study provides additional support for immunochemical similarities betw een Al-induced NFD in rabbits and the neurofibrillary tangles in human subjects with Alzheimer's disease. (C) 1997 Elsevier Science B.V.