TY - JOUR
T1 - The apoE receptor apoER2 is involved in the maintenance of efficient synaptic plasticity
AU - Petit-Turcotte, Caroline
AU - Aumont, Nicole
AU - Beffert, Uwe
AU - Dea, Doris
AU - Herz, Joachim
AU - Poirier, Judes
N1 - Funding Information:
Authors would like to thank Wen-Ling Niu for her excellent technical assistance. This work was supported by the Alzheimer Society of Canada (JP) and the Canadian Institute for Health Research (JP, UB, CPT), The Human Frontier Science Program (UB) and the National Institutes of Health (HL20948, NS43408 and HL63762) (JH), the Alzheimer Association (JH) and the Perot Family Foundation (JH).
PY - 2005/2
Y1 - 2005/2
N2 - ApoER2 is one of the major receptors for ApoE in the brain, and has been shown to be involved not only in lipoprotein endocytosis, as other members of the LDL receptor family of receptors, but also in various cellular functions such as signalling and cellular guidance. By using a model of synaptic plasticity in mice lacking none, one or two alleles of the apoER2 gene, we investigated the implication of such a receptor deficiency on the remodelling process. Our results indicate that animals lacking apoER2 express higher levels of brain APP, as well as both key amyloid peptides, while apoE levels are slightly lower. Following entorhinal cortex lesioning, apoE levels increase in the deafferented hippocampus, while a delay in the increase of APP was observed. Hippocampal amyloid levels are also increased in response to the lesion, and highly potentiated by the complete absence of apoER2 gene. The results suggest a significant role for apoER2 in signalling various proteins in response to massive deafferentation and may participate in maintaining efficient synaptic plasticity and dendritic remodelling.
AB - ApoER2 is one of the major receptors for ApoE in the brain, and has been shown to be involved not only in lipoprotein endocytosis, as other members of the LDL receptor family of receptors, but also in various cellular functions such as signalling and cellular guidance. By using a model of synaptic plasticity in mice lacking none, one or two alleles of the apoER2 gene, we investigated the implication of such a receptor deficiency on the remodelling process. Our results indicate that animals lacking apoER2 express higher levels of brain APP, as well as both key amyloid peptides, while apoE levels are slightly lower. Following entorhinal cortex lesioning, apoE levels increase in the deafferented hippocampus, while a delay in the increase of APP was observed. Hippocampal amyloid levels are also increased in response to the lesion, and highly potentiated by the complete absence of apoER2 gene. The results suggest a significant role for apoER2 in signalling various proteins in response to massive deafferentation and may participate in maintaining efficient synaptic plasticity and dendritic remodelling.
KW - AD
KW - APP
KW - Alzheimer's disease
KW - Apolipoprotein E receptor
KW - Aβ
KW - ECL
KW - Synaptic plasticity
KW - amyloid precursor protein
KW - amyloid-beta peptide
KW - apoE
KW - apoE receptor type 2
KW - apoER2
KW - apolipoprotein E
KW - entorhinal cortex lesioning
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U2 - 10.1016/j.neurobiolaging.2004.04.007
DO - 10.1016/j.neurobiolaging.2004.04.007
M3 - Article
C2 - 15582748
AN - SCOPUS:10044273221
SN - 0197-4580
VL - 26
SP - 195
EP - 206
JO - Neurobiology of Aging
JF - Neurobiology of Aging
IS - 2
ER -