title: Coexistences of insulin signaling-related proteins and choline acetyltransferase in neurons.
abstract: Type 2 diabetes recently has been identified as a risk factor for developing Alzheimer's disease (AD). The main reason for this appears to be insulin signaling failure in the brain. Furthermore, cholinergic neurons are particularly affected in the brains of AD patients. The aim of the present study is to investigate if insulin signaling-related proteins are co-located with cholinergic neuron in the CA1 region of hippocampus of mice, which could explain the early loss of cholinergic neurons in AD. Using immunohistochemistry, the insulin signaling-related proteins, such as insulin receptor (InsR), insulin receptor substrate-1 (IRS-1), protein kinase B (PKB, also named Akt), glycogen synthase kinase-3beta (GSK-3beta) and insulin-degrading enzyme (IDE) were analysed. Choline acetyltransferase (ChAT) was selected as a marker of cholinergic neurons. In the CA1 region of hippocampus of mice, several of the insulin signaling-related proteins we had chosen are co-located with ChAT, and most double immunoreactive positive cells were pyramidal cells. The coexistences indicated that the insulin signaling may play an important part in the activities of cholinergic neurons, and the impairment of the pathway may be important in the mechanisms that underlie neurodegeneration in AD.
authors.affiliation: Central Laboratory, Xuanwu Hospital of Capital Medical University, Key Laboratory for Neurodegenerative Disease of Ministry of Education, #45 Changchun Street, Xuanwu District, Beijing 100053, China.
authors.forename: Hongjuan
authors.initials: H
authors.lastname: Wang
authors.forename: Rong
authors.initials: R
authors.lastname: Wang
authors.forename: Zhiwei
authors.initials: Z
authors.lastname: Zhao
authors.forename: Zhijuan
authors.initials: Z
authors.lastname: Ji
authors.forename: Shiming
authors.initials: S
authors.lastname: Xu
authors.forename: Christian
authors.initials: C
authors.lastname: Holscher
authors.forename: Shuli
authors.initials: S
authors.lastname: Sheng
mesh_terms: D000818:Animals; D002795:Choline O-Acetyltransferase / Q000378:metabolism*; D005455:Fluorescent Antibody Technique; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D006624:Hippocampus / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism; D007339:Insulysin / Q000378:metabolism; D008297:Male; D051379:Mice; D009474:Neurons / Q000201:enzymology / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D017966:Pyramidal Cells / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D002795:Choline O-Acetyltransferase; D011972:Receptor, Insulin; D000071679:Glycogen Synthase Kinase 3 beta; C000605507:Gsk3b protein, mouse; D051057:Proto-Oncogene Proteins c-akt; D038362:Glycogen Synthase Kinase 3; D007339:Insulysin