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Amyloid beta-peptide effects on synaptosomes from apolipoprotein E-deficient mice
J N Keller1, C M Lauderback, D A Butterfield
1Sanders-Brown Center on Aging, University of Kentucky, Lexington 40536-0230, USA.
Journal of Neurochemistry
|March 29, 2000
Summary
Apolipoprotein E (apoE) protects brain synapses from damage. Mice lacking apoE showed increased oxidative stress and mitochondrial issues when exposed to amyloid beta, highlighting apoE's role in synaptic homeostasis.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Apolipoprotein E (apoE) is found in the brain and influences neurophysiology.
- Emerging research suggests apoE's involvement in synaptic plasticity and homeostasis.
- Genetic factors and environment modulate apoE's role in neurological events.
Purpose of the Study:
- To investigate the role of apoE in maintaining synaptic homeostasis.
- To analyze synaptosomes from apoE knockout (KO) mice for potential contributions of apoE.
Main Methods:
- Preparation of cerebrocortical synaptosomes from apoE KO and wild-type mice.
- Assessment of basal reactive oxygen species, mitochondrial function, and caspase activity.
- Evaluation of synaptosomes after exposure to amyloid beta-peptide [Abeta(1-40)].
Main Results:
- ApoE KO synaptosomes showed elevated oxidative stress, mitochondrial dysfunction, and caspase activation post-Abeta(1-40) exposure compared to wild-type.
- Synaptosomal membranes from apoE KO mice exhibited increased fluidity and lipid peroxidation.
- Basal levels of oxidative stress, mitochondrial function, and caspase activity were similar between apoE KO and wild-type mice.
Conclusions:
- Apolipoprotein E plays a crucial role in maintaining synaptic homeostasis.
- ApoE attenuates oxidative stress, caspase activation, and mitochondrial dysfunction in synapses.
- The absence of apoE exacerbates synaptotoxicity induced by amyloid beta-peptide.