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Apoptosis is secondary to non-apoptotic axonal degeneration in neurons exposed to Aβ in distal axons

Song, Mee-Sook, Saavedra, Lucila, de Chaves, Elena I. Posse·2006·Neurobiology of Aging
DOI 10.1016/j.neurobiolaging.2005.06.007
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Abstract

The goal of this study was to assess if neurons exposed to amyloid-beta peptide (Abeta) exclusively in distal axons, undergo apoptosis. This is relevant to the loss of cholinergic neurons in Alzheimer's disease. Using a three-compartmented culture system for rat sympathetic neurons, we demonstrate that exposure of axons to Abeta1-42 activates an independent destruction program in axons, which leads to nuclear apoptosis. Abeta-induced axonal degeneration does not involve local caspase activation, but causes caspase activation in cell bodies. Accordingly, inhibition of caspase activation blocks Abeta-induced apoptosis but not axonal degeneration. In agreement with previous suggestions that disruption of nerve growth factor (NGF)-mediated signaling might contribute to the loss of cholinergic neurons, we found that provision of NGF to cell bodies protects sympathetic neurons from Abeta-induced apoptosis. However, our data indicate that Abeta-induced axonal degeneration follows a mechanism different than that activated by NGF withdrawal. Only Abeta-induced axonal degeneration is prevented by the calpain inhibitor calpastatin and is insensitive to the inhibitor of the ubiquitin-proteasome system MG132. Importantly, inhibition of Abeta-induced axonal degeneration by calpastatin prevents nuclear apoptosis.

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Metadata

Authors
Song, M.-S., Saavedra, L., & de Chaves, E. I. P.
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2006-09
Volume
27
Issue
9
Pages
1224-1238
ISSN
0197-4580
DOI
10.1016/j.neurobiolaging.2005.06.007
Cited by
40
References
7
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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