Juraj Sprung1, David O Warner2, David S Knopman3, Ronald C Petersen3, Michelle M Mielke4, Clifford R Jack5, Val J Lowe5, David P Martin2, Andrew C Hanson6, Darrell R Schroeder7, Scott A Przybelski6, Phillip J Schulte6, Toby N Weingarten2, Prashanthi Vemuri5. 1. Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN, USA. Electronic address: sprung.juraj@mayo.edu. 2. Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN, USA. 3. Department of Neurology, Mayo Clinic, Rochester, MN, USA. 4. Department of Neurology, Mayo Clinic, Rochester, MN, USA; Health Sciences Research, Division of Epidemiology, Mayo Clinic, Rochester, MN, USA. 5. Department of Radiology, Mayo Clinic, Rochester, MN, USA. 6. Health Sciences Research, Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, MN, USA. 7. Health Sciences Research, Division of Epidemiology, Mayo Clinic, Rochester, MN, USA.
Abstract
BACKGROUND: Exposure to surgery with general anaesthesia (surgery/GA) is associated with cortical atrophy, but the aetiology remains unknown. Amyloid-β (Aβ) deposition is one of the hallmark pathological characteristics of Alzheimer's disease (AD). We examined brain Aβ burden in study participants exposed to surgery/GA. METHODS: We performed a cross-sectional analysis of residents of Olmsted County, MN, USA, in the Mayo Clinic Study of Aging who were aged 70-97 yr and underwent measurement of (i) brain Aβ with Pittsburgh compound B positron emission tomography (PiB PET), (ii) brain glucose metabolism with 18-fluorodeoxyglucose (FDG) PET, and (iii) temporal cortical thickness with MRI. Separate analyses were performed with exposure to surgery/GA, defined as occurring after age 40 yr, and with exposure to surgery/GA, defined as occurring within 20 yr before neuroimaging. Imaging measurements were compared between participants who were exposed to surgery/GA vs not exposed. RESULTS: Of the 2563 participants, 585 had PET scans. Regardless of the definition used to quantify exposure, no significant associations were detected between exposure and either global PiB PET or FDG PET. In contrast, exposure to surgery/GA was associated with an increased likelihood of abnormal cortical thinning: odds ratio (OR)=1.98 (95% confidence interval [CI]: 1.19-3.31); P=0.010 in those exposed after age 40 yr, and OR=1.64 (95% CI: 1.05-2.55); P=0.029 in those exposed in the prior 20 yr. CONCLUSIONS: Exposure to surgery/GA is not associated with increases in cortical amyloid deposition. This finding suggests that the modest cortical thinning associated with surgery/GA is not related to AD pathology, but rather is caused by other processes.
BACKGROUND: Exposure to surgery with general anaesthesia (surgery/GA) is associated with cortical atrophy, but the aetiology remains unknown. Amyloid-β (Aβ) deposition is one of the hallmark pathological characteristics of Alzheimer's disease (AD). We examined brain Aβ burden in study participants exposed to surgery/GA. METHODS: We performed a cross-sectional analysis of residents of Olmsted County, MN, USA, in the Mayo Clinic Study of Aging who were aged 70-97 yr and underwent measurement of (i) brain Aβ with Pittsburgh compound B positron emission tomography (PiB PET), (ii) brain glucose metabolism with 18-fluorodeoxyglucose (FDG) PET, and (iii) temporal cortical thickness with MRI. Separate analyses were performed with exposure to surgery/GA, defined as occurring after age 40 yr, and with exposure to surgery/GA, defined as occurring within 20 yr before neuroimaging. Imaging measurements were compared between participants who were exposed to surgery/GA vs not exposed. RESULTS: Of the 2563 participants, 585 had PET scans. Regardless of the definition used to quantify exposure, no significant associations were detected between exposure and either global PiB PET or FDG PET. In contrast, exposure to surgery/GA was associated with an increased likelihood of abnormal cortical thinning: odds ratio (OR)=1.98 (95% confidence interval [CI]: 1.19-3.31); P=0.010 in those exposed after age 40 yr, and OR=1.64 (95% CI: 1.05-2.55); P=0.029 in those exposed in the prior 20 yr. CONCLUSIONS: Exposure to surgery/GA is not associated with increases in cortical amyloid deposition. This finding suggests that the modest cortical thinning associated with surgery/GA is not related to AD pathology, but rather is caused by other processes.
Keywords:
Alzheimer's disease; MRI; Mayo Clinic Study of Aging; brain amyloid; general anaesthesia; neurodegeneration; positron emission tomography; surgery
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