Crotonaldehyde accumulates in glial cells of Alzheimer's disease brain.
Kawaguchi-Niida M, Shibata N, Morikawa S, Uchida K, Yamamoto T, Sawada
T, Kobayashi M
Acta Neuropathol (Berl). 2006 Mar 15;

Several studies have documented the involvement of oxidative stress
represented by lipid peroxidation in the pathogenesis of Alzheimer's
disease (AD). To test whether the highly reactive carbonyl
crotonaldehyde (CRA), generated during lipid peroxidation, is involved
in AD, we performed an immunohistochemical analysis in AD and
age-matched control hippocampi using a specific antibody against
protein-bound CRA (P-CRA). In the AD cases, P-CRA immunoreactivity was
preferentially localized in reactive astrocytes and microglia around
senile plaques (SPs) and those present in the neuropil, while it was
weakly detectable in neurons and neurofibrillary tangles. P-CRA
immunoreactivity was also localized in all portions of diffuse SPs and
the dystrophic neurites of neuritic and classical SPs, but was
undetectable in amyloid cores. Age-matched controls showed P-CRA
immunoreactivity only very weakly in neurons. In contrast to P-CRA,
immunoreactivities for protein-bound acrolein and 4-hydroxy-2-nonenal
were mainly localized to neurons and rarely seen in glial cells. Our
results suggest that increased oxidative stress and CRA formation in
glial cells is implicated in the disease processes of AD.

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