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Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus
Published on: June 17, 2015
RAGE does not affect amyloid pathology in transgenic ArcAbeta mice
Ivana Vodopivec1, Arnaud Galichet, Marlen Knobloch
1Division of Psychiatry Research, University of Zurich, CH-8008 Zurich, Switzerland. ivana.vodopivec @ bli.uzh.ch
Neuro-Degenerative Diseases
|February 11, 2010
Summary
Deleting the receptor for advanced glycation end products (RAGE) in a mouse model of Alzheimer's disease (AD) increased insulin-degrading enzyme activity but did not prevent cognitive decline or amyloid-beta (Abeta) accumulation.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Alzheimer's disease (AD) involves brain accumulation of amyloid-beta (Abeta) peptides, triggering pathological processes.
- The receptor for advanced glycation end products (RAGE) binds Abeta and is implicated in AD pathogenesis.
Purpose of the Study:
- To investigate the impact of RAGE deletion on Abeta-related pathology in a mouse model of AD.
Main Methods:
- Crossed RAGE knockout mice with arcAbeta mice (transgenic for Swedish and Arctic Abeta precursor protein mutations).
- Assessed Abeta levels, brain deposition, enzyme activities, protein expression, microglia characteristics, and cognitive performance at 6 and 12 months.
Main Results:
- RAGE deletion reduced cortical and hippocampal Abeta levels and increased insulin-degrading enzyme activity at 6 months.
- Cognitive decline and age-related Abeta accumulation were not prevented by RAGE deletion.
- No differences in microglia area or morphology were observed between RAGE(-/-)/arcAbeta and arcAbeta mice.
Conclusions:
- Absence of RAGE increased insulin-degrading enzyme activity but did not ameliorate cognitive deficits, Abeta accumulation, or microglial activation in this AD mouse model.
