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White matter degeneration is a frequent phenomenon found in Alzheimer's disease
(AD) apart from the well-known lesions in certain grey matter areas such as cortex and
hippocampus. However its pathogenesis has not been fully established. Therefore, the aim of
this work was to assess the effects of Aβ 1-42 in rat corpus callosum from 6 hr upto 2 weeks
using immunocytochemistry since amyloid deposits can be found in CC of AD patients.
Administration of 1 nmol of Aβ 1-42 into corpus callosum resulted in considerable damage to
axons, as evidenced by the loss of neurofilament-immunoreactive fibers at time points of 6
hrs and 7 days post-injection. Significant damage was also evident to myelin (using Luxol fast
blue myelin staining) and oligodendrocytes (using CC1 irnmunocytochemistry); in the latter
case marked caspase-3 immunoreactivity was demonstrated in the CC 1-immunoreactive
oligodendrocytes. Additionally, the numbers of GFAP-immunoreactive astrocytes and OX-
42/OX-6-immunoreactive microglia were markedly increased following Aβ 1-42 injection.
These findings suggest that Aβ 1-42 plays an important pathophysiological role in white
matter damage and one possible mechanism of oligodendroglial death is through activation of
caspase-3. This is the first finding on Aβ 1-42-induced toxicity in corpus callosum in vivo
which could provide a potential new model for the study of white matter damage in AD.
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