Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11588
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dc.contributor.authorVerdile, G-
dc.contributor.authorLaws, Simon M-
dc.contributor.authorHenley, D-
dc.contributor.authorAmes, David-
dc.contributor.authorBush, Ashley I-
dc.contributor.authorEllis, Kathryn A-
dc.contributor.authorFaux, N G-
dc.contributor.authorGupta, V B-
dc.contributor.authorLi, Q-X-
dc.contributor.authorMasters, Colin L-
dc.contributor.authorPike, Kerryn E-
dc.contributor.authorRowe, Christopher C-
dc.contributor.authorSzoeke, Cassandra-
dc.contributor.authorTaddei, K-
dc.contributor.authorVillemagne, Victor L-
dc.contributor.authorMartins, Ralph N-
dc.date.accessioned2015-05-16T01:12:13Z
dc.date.available2015-05-16T01:12:13Z
dc.date.issued2012-10-23-
dc.identifier.citationMolecular Psychiatry 2012; 19(1): 69-75en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11588en
dc.description.abstractTestosterone and gonadotropins have been associated with cognitive decline in men and the modulation of β amyloid (Aβ) metabolism. The relatively few studies that have investigated whether changes in one or a combination of these hormones influence Aβ levels have focused primarily on plasma Aβ(1-40) and not on the more pathogenic Aβ(1-42). Currently, no study has investigated whether these hormones are associated with an increase in brain amyloid deposition, ante mortem. Through the highly characterised Australian imaging, biomarkers and lifestyle study, we have determined the impact of these hormones on plasma Aβ levels and brain amyloid burden (Pittsburgh compound B (PiB) retention). Spearman's rank correlation and linear regression analysis was carried out across the cohort and within subclassifications. Luteinizing hormone (LH) was the only variable shown, in the total cohort, to have a significant impact on plasma Aβ(1-40) and Aβ(1-42) levels (beta=0.163, P<0.001; beta=0.446, P<0.001). This held in subjective memory complainers (SMC) (Aβ(1-40); beta=0.208, P=0.017; Aβ(1-42); beta=0.215, P=0.017) but was absent in mild cognitive impairment (MCI) and Alzheimer's disease (AD) groups. In SMC, increased frequency of the APOE-ɛ4 allele (beta=0.536, P<0.001) and increasing serum LH levels (beta=0.421, P=0.004) had a significant impact on PiB retention. Whereas in MCI, PiB retention was associated with increased APOE-ɛ4 allele copy number (beta=0.674, P<0.001) and decreasing calculated free testosterone (beta=-0.303, P=0.043). These findings suggest a potential progressive involvement of LH and testosterone in the early preclinical stages of AD. Furthermore, these hormones should be considered while attempting to predict AD at these earliest stages of the disease.en
dc.language.isoenen
dc.subject.otherAgeden
dc.subject.otherAged, 80 and overen
dc.subject.otherAlzheimer Disease.metabolism.radionuclide imagingen
dc.subject.otherAmyloid beta-Peptides.metabolismen
dc.subject.otherAniline Compounds.diagnostic useen
dc.subject.otherApolipoproteins E.geneticsen
dc.subject.otherCohort Studiesen
dc.subject.otherGonadotropins.metabolismen
dc.subject.otherHumansen
dc.subject.otherLinear Modelsen
dc.subject.otherMaleen
dc.subject.otherMemory Disorders.metabolism.radionuclide imagingen
dc.subject.otherMiddle Ageden
dc.subject.otherMild Cognitive Impairment.metabolism.radionuclide imagingen
dc.subject.otherNeuropsychological Testsen
dc.subject.otherPeptide Fragments.metabolismen
dc.subject.otherPositron-Emission Tomographyen
dc.subject.otherPsychiatric Status Rating Scalesen
dc.subject.otherRisk Factorsen
dc.subject.otherStatistics, Nonparametricen
dc.subject.otherTestosterone.metabolismen
dc.subject.otherThiazoles.diagnostic useen
dc.titleAssociations between gonadotropins, testosterone and β amyloid in men at risk of Alzheimer's disease.en
dc.typeJournal Articleen
dc.identifier.journaltitleMolecular psychiatryen
dc.identifier.affiliationDepartment of Nuclear Medicine & Centre for PET, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationMental Health Research Institute, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationSchool of Medicine and Pharmacology, University of Western Australia, Crawley, Western Australia, Australiaen
dc.identifier.affiliationNational Ageing Research Institute, Parkville, Victoria, Australiaen
dc.identifier.affiliationCentre for Neuroscience, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationDepartment of Pathology, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationCSIRO, Parkville, Victoria, Australiaen
dc.identifier.affiliationCentre of Excellence for Alzheimer's Disease Research & Care, School of Medical Sciences, Edith Cowan University, Joondalup, Western Australia, Australiaen
dc.identifier.affiliationDepartment of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australiaen
dc.identifier.affiliationAcademic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, St Vincent's Aged Psychiatry Service, St George's Hospital, Melbourne, Victoria, Australiaen
dc.identifier.affiliationCo-operative Research Centre for Mental Health, http://www.mentalhealthcrc.comen
dc.identifier.affiliationSchool of Psychological Science, La Trobe University, Bundoora, Victoria Australiaen
dc.identifier.affiliationSir James McCusker Alzheimer's Disease Research Unit (Hollywood Private Hospital), Perth, Western Australia, Australiaen
dc.identifier.affiliationDepartment of Nuclear Medicine & Centre for PET, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationCo-operative Research Centre for Mental Health, http://www.mentalhealthcrc.com.en
dc.identifier.doi10.1038/mp.2012.147en
dc.description.pages69-75en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/23089633en
dc.contributor.corpauthorAIBL Research Groupen
dc.type.contentTexten
dc.type.austinJournal Articleen
local.name.researcherMasters, Colin L
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptMolecular Imaging and Therapy-
crisitem.author.deptMolecular Imaging and Therapy-
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