aDepartment of Pathology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.
bDepartment of Medical Chemistry and Biochemistry, Second Medical School, Charles University, Prague.
cCentre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Canada.
dSchool of Health Sciences, Gunma University, Maebashi.
eDepartment of Pathology, Otto-von-Guericke-University, Magdeburg, Germany.
*E-mail: skuldee@cvm.okstate.edu
The present study was planned to search for an animal model to study the pathogenesis and therapeutics of Alzheimer's disease. A total of 25 dogs were taken for this study and the distribution of antigens were investigated using mouse monoclonal antibodies against APP (C-terminal), tau (AT8), Abeta (8‒17; 33‒40 and 37‒42), 4-hydroxynonenal protein (an oxidative damage product) and rabbit antibody against advanced glycation end products (AGE). The amounts of reaction product were analysed semiquantitatively. Moreover, for oxidative damage brain extracts were analyzed for lipofuscin-like compounds by tridimensional fluorescence spectroscopy. APP-positive cells were recognized regardless of the age of dogs. Amyloid deposition was noticed in cerebral blood vessels and brain parenchyma of the aged dogs. Some dispersed tau-positive neurons were found in increasing numbers in the cerebral cortex and basal nuclei of the older dogs and an AGE-positive signal was seen in degenerating neurons, astrocytes, macrophages and cerebral blood vessel walls of the older animals. Brain extracts revealed a clear difference between age groups excitation patterns of lipofuscin-like pigments.
Canine, Amyloid Alzheimer's disease, Brain
