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Title of Journal: Acta Neuropathol

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Abbravation: Acta Neuropathologica

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Springer-Verlag

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DOI

10.1007/978-3-540-77226-2_42

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1432-0533

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Oxidative damage in the olfactory system in Alzhei

Authors: George Perry Rudy J Castellani Mark A Smith Peggy L R Harris Zvezdana Kubat Kasra Ghanbari Paul K Jones Giovanni Cordone Massimo Tabaton Benjamin Wolozin Hossein Ghanbari
Publish Date: 2003/08/29
Volume: 106, Issue: 6, Pages: 552-556
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Abstract

Increased oxidative damage is a prominent and early feature of vulnerable neurons in Alzheimers disease AD However while damage to proteins sugars lipids nucleic acids and organelles such as lysosomes mitochondria and endoplasmic reticulum are evident the source of increased reactive oxygen species has not been determined Furthermore a major limitation in further determining the source as well as finding a means to arrest damage is the paucity of cellular models directly homologous to AD since the vulnerable neurons of the brain in AD cannot be studied in vitro Here we examined the olfactory epithelium in situ to see if neurons there exhibit a similar pathological oxidative balance to vulnerable neurons in AD In biopsy specimens eight AD and three controls we found that neurons and also the surrounding epithelial cells show an increase in oxidative damage for a subset of the markers increased in the brain of cases of AD Lipid peroxidation and heme oxygenase1 a stress response protein were increased while nucleic acid or protein oxidation demonstrated in vulnerable neurons in AD were not increased These findings highlight the systemic nature of oxidative abnormalities in AD but that different cell types may express this abnormality by a different array of oxidative stress markers supporting the potential for using olfactory neurons or other cells derived from AD patients in culture to understand the mechanistic basis for increased oxidative damage in AD and as a model to screen compounds for therapeutic intervention

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