The autocrine regulation of insulin-like growth factor-1 in human brain of Alzheimer's disease.

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dc.contributor.author Kang, Dali
dc.contributor.author Waldvogel, Henry J
dc.contributor.author Wang, Ao
dc.contributor.author Fan, Dawei
dc.contributor.author Faull, Richard LM
dc.contributor.author Curtis, Maurice A
dc.contributor.author Shorten, Paul R
dc.contributor.author Guan, Jian
dc.coverage.spatial England
dc.date.accessioned 2021-09-21T22:17:10Z
dc.date.available 2021-09-21T22:17:10Z
dc.date.issued 2021-5
dc.identifier.issn 0306-4530
dc.identifier.uri https://hdl.handle.net/2292/56613
dc.description.abstract <h4>Background</h4>Insulin-like growth factor (IGF) binding protein (IGFBP)-3 and cyclic Glycine-Proline (cGP) regulate circulating IGF-1 function that is associated with cognition. The association between IGF-1 function and Alzheimer's disease (AD) remains inconclusive. This study evaluated the changes of IGFBPs and cGP, and their effects on the bioavailability and function of IGF-1 in human brain of AD cases.<h4>Methods</h4>Using biological and mathematic analysis we measured the concentrations of total, bound and unbound forms of IGF-1, IGFBPs and cGP in the inferior-frontal gyrus and middle-frontal gyrus of human AD (n = 15) and control cases (n = 15). The association between the changes of total concentration of these peptides and total protein concentration in brain tissues were also analyzed.<h4>Results</h4>The unbound bioavailable IGF-1 was lower whereas the bound cGP and IGFBP-3 were higher in AD than the control cases. Total protein that was lower in AD than control cases, was negatively associated with cGP concentration of control cases and with IGFBP-3 concentration of AD cases.<h4>Conclusions</h4>The results provide direct evidence for IGF-1 deficiency in AD brain due to lower bioavailable IGF-1. The increase of bound IGFBP-3 impaired autocrine regulation. The increase of bound cGP is an autocrine response to improve the bioavailability and function of IGF-1 in AD brain.<h4>Availability of data and material</h4>All data generated or analysed during this study are included in this published article. Additional datasets analysed during the current study available from the corresponding author on reasonable request.
dc.format.medium Print-Electronic
dc.language eng
dc.publisher Elsevier BV
dc.relation.ispartofseries Psychoneuroendocrinology
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher.
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm
dc.subject Alzheimer’s diseases (AD)
dc.subject Autocrine regulation
dc.subject Cyclic Glycine-Proline (cGP)
dc.subject Human brains
dc.subject IGF binding protein (IGFBP)s
dc.subject Insulin-like growth factor-1 (IGF-1)
dc.subject Science & Technology
dc.subject Life Sciences & Biomedicine
dc.subject Endocrinology & Metabolism
dc.subject Neurosciences
dc.subject Psychiatry
dc.subject Neurosciences & Neurology
dc.subject Autocrine regulation
dc.subject Insulin-like growth factor-1 (IGF-1)
dc.subject IGF binding protein (IGFBP)s
dc.subject Cyclic Glycine-Proline (cGP)
dc.subject Human brains
dc.subject CYCLIC GLYCINE-PROLINE
dc.subject IGF-I
dc.subject BINDING
dc.subject SIMULATION
dc.subject TAU
dc.subject 11 Medical and Health Sciences
dc.subject 17 Psychology and Cognitive Sciences
dc.title The autocrine regulation of insulin-like growth factor-1 in human brain of Alzheimer's disease.
dc.type Journal Article
dc.identifier.doi 10.1016/j.psyneuen.2021.105191
pubs.begin-page 105191
pubs.volume 127
dc.date.updated 2021-08-11T02:12:39Z
dc.rights.holder Copyright: The author en
pubs.author-url https://www.ncbi.nlm.nih.gov/pubmed/33706042
pubs.publication-status Published
dc.rights.accessrights http://purl.org/eprint/accessRights/RetrictedAccess en
pubs.subtype Journal Article
pubs.elements-id 844149
dc.identifier.eissn 1873-3360
dc.identifier.pii S0306-4530(21)00065-2
pubs.number 105191


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