S100b counteracts neurodegeneration of rat cholinergic neurons in brain slices after oxygen-glucose deprivation.
Alzheimer's disease is a severe chronic neurodegenerative disorder characterized by beta-amyloid plaques, tau pathology, cerebrovascular damage, inflammation, reactive gliosis, and cell death of cholinergic neurons. The aim of the present study is to test whether the glia-derived molecule S100b can counteract neurodegeneration of cholinergic neurons after oxygen-glucose deprivation (OGD) in organotypic brain slices of basal nucleus of Meynert. Our data showed that 3 days of OGD induced a marked decrease of cholinergic neurons (60% of control), which could be counteracted by 50 mug/mL recombinant S100b. The effect was dose and time dependent. Application of nerve growth factor or fibroblast growth factor-2 was less protective. C-fos-like immunoreactivity was enhanced 3 hours after OGD indicating metabolic stress. We conclude that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.
Laboratory of Psychiatry and Exp. Alzheimer's Research, Department of Psychiatry and Psychotherapy, Innsbruck Medical University, Anichstra beta e 35, 6020 Innsbruck, Austria.
Daniela
D
Serbinek
Celine
C
Ullrich
Michael
M
Pirchl
Tanja
T
Hochstrasser
Rainald
R
Schmidt-Kastner
Christian
C
Humpel