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  • 1
    ISSN: 1432-0533
    Keywords: Key words Aging ; Animal model ; Cortex ; Microtubule-associated protein tau ; Hyperphosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aged individuals of mammalian species displaying hyperphosphorylated tau protein may be suitable natural models for investigating neurodegenerative alterations occurring, for example, in Alzheimer’s disease. Therefore, autoptic tissue from the entorhinal, motor and prefrontal cortices of 14 mammalian species was screened using the monoclonal antibody AT8, which is directed against a phosphorylated epitope of human tau and applicable to the tissues of aged domestic animals, as shown in previous studies. AT8-immunoreactive neuronal processes and perikarya were revealed in Campbell’s guenon, rhesus monkey, baboon, rabbit, spectacled bear, guanaco, reindeer and bison. Signs for considerable neuropathological alterations in aged bisons also included neuropil threads, whereas AT8 immunoreactivity in the other species was only sparsely scattered. Hyperphosphorylated tau in the brain of an 28-year-old rhesus monkey was also detected by AT100, PHF-1 and TG-3 antibodies, but only in the hippocampal formation and entorhinal cortex, which are known as starting point for tangle spreading in the cortex of Alzheimer patients.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 60 (1985), S. 527-534 
    ISSN: 1432-1106
    Keywords: Electron microscopy ; Lateral geniculate nucleus ; Mouse ; Mutant ; Microphthalmia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ultrastructure of the dorsal lateral geniculate nucleus (dLGN) of microphthalmic mice is described in affected white homozygotes (mi/mi) and their apparently normal grey littermates. In the dLGN of mi/mi animals populations of apparently normal axon terminals were observed, including some with flattened synaptic vesicles and other small terminals with round vesicles and dark mitochondria (RSD), possibly of cortico-thalamic origin, just as in normal mice. However, no typical large retinal endings with round vesicles and pale mitochondria (RLP) are visible. Instead they appear to be replaced by other large boutons with round vesicles and dark mitochondria (RLD). Eye enucleation does not cause degeneration of these RLD terminals. In apparently normal grey littermates RLP terminals are present and they degenerate when an eye is enucleated. But RLD endings are also found in these animals, and never degenerate after enucleation. The origin of the RLD terminals is unclear but seems not to be cortical. These findings are compared with those of Cullen and Kaiserman-Abramof (1976) in a different strain (ZRDCT-An) of anophthalmic mouse in which they found large replacement terminals similar to our RLD boutons.
    Type of Medium: Electronic Resource
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