4.5 Article

Brain Regional Glucose Metabolism, Neuropsychiatric Symptoms, and the Risk of Incident Mild Cognitive Impairment: The Mayo Clinic Study of Aging

期刊

AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
卷 29, 期 2, 页码 179-191

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jagp.2020.06.006

关键词

Neuropsychiatric symptoms; FDG-PET; mild cognitive impairment; Alzheimer Disease

资金

  1. NIH grant: National Institute on Aging [R01 AG057708, U01 AG006786, P50 AG016574, R01 AG034676, R01 AG011378, R01 AG041851]
  2. NIH grant: National Institute of Mental Health [K01 MH068351]
  3. National Institute of Neurological Disorders and Stroke [R01 NS097495]
  4. Robert Wood Johnson Foundation
  5. Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program
  6. GHR Foundation
  7. Mayo Foundation for Medical Education and Research
  8. National Program of Sustainability II (MEYS CR) [LQ1605]
  9. Edli Foundation
  10. Arizona Alzheimer's Consortium

向作者/读者索取更多资源

The combination of NPS with regional glucose hypometabolism is associated with an increased risk of incident MCI, with fluorodeoxyglucose positron emission tomography appearing to be a stronger driving force of cognitive decline than NPS.
Objective: The authors conducted a prospective cohort study to examine the risk of incident mild cognitive impairment (MCI) as predicted by baseline neuropsychiatric symptoms (NPS) and brain regional glucose metabolic dysfunction. Methods: About 1,363 cognitively unimpaired individuals (52.8% males) aged >= 50 years were followed for a median of 4.8 years to the outcome of incident MCI. NPS were assessed using Beck Depression and Anxiety Inventories and Neuropsychiatric Inventory Questionnaire. Glucose hypometabolism was measured by fluorodeoxyglucose positron emission tomography and defined as standardized uptake value ratio <= 1.47 in regions typically affected in Alzheimer disease. Cox proportional hazards models were adjusted for age, sex, education, and APOE epsilon 4 status. Results: Participants with regional glucose hypometabolism and depression (Beck Depression Inventory-II >= 13) had a more than threefold increased risk of incident MCI (hazard ratio [95% confidence interval], 3.66 [1.75, 7.65], p <0.001, chi(2) = 11.83, degree of freedom [df] =1) as compared to the reference group (normal regional glucose metabolism and no depression), and the risk was also significantly elevated (7.21 13.54, 14.7], p <0.001, f = 29.68, df =1) for participants with glucose hypometabolism and anxiety (Beck Anxiety Inventory >= 10). Having glucose hypometabolism and >= 1 NPS (3. 74 12.40, 5.82], p <0.001, chi(2) = 34. 13, df =1) or >= 2 NPS (3.89 12.20, 686], p <0.001, chi(2) = 21.92, df = 1) increased the risk of incident MCI by more than three times, and having >= 3 NPS increased the risk by more than four times (4.12 12.03, 8.3 7], p <0.001, chi(2) = 15.39, df =1). Conclusion: Combined presence of NPS with regional glucose hypometabolism is associated with an increased risk of incident MCI, with fluorodeoxyglucose positron emission tomography appearing to be a stronger driving force of cognitive decline than NPS.

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