Neuropsychiatric symptoms as predictors of MCI and dementia: Epidemiologic evidence

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1 16th Annual MCI Symposium January 20, 2018 Miami, FL Neuropsychiatric symptoms as predictors of MCI and dementia: Epidemiologic evidence Yonas E. Geda, MD, MSc Professor of Neurology and Psychiatry Consultant, Departments of Psychiatry & Psychology, and Neurology Mayo Clinic, Scottsdale, Arizona 2015 MFMER slide-1

2 Conflict of interest Dr Geda served as an advisory board member to Lundbeck in March of Dr Geda is funded by the European Union, NIH and the Edward and Lili foundation (Hague, the Netherlands) 2015 MFMER slide-2

3 Outline Introduction: Neuropsychiatric symptoms (NPS), MCI and dementia Study 1: From normal aging to incident MCI as predicted by baseline NPS (Geda et al. Am J Psychiatry. 2014) Study 2: From MCI to incident dementia as predicted by baseline NPS (Pink et al., Neurology. 2015) NPS and neuroimaging biomarkers of presymptomatic AD 2015 MFMER slide-3

4 Introduction: NPS, MCI and dementia Neuropsychiatric symptoms (NPS) are highly prevalent in patients with MCI (Lyketsos, JAMA 2002; Geda, Arch Gen Psychiatry 2008) Prevalence of NPS in MCI ranges from 35% - 85% (Monastero, J Alzheimers Dis 2009; Review) Most common NPS are apathy, depression, and irritability in both Cardiovascular Health Study (Lyketsos, JAMA 2002) and Mayo Clinic Study of Aging (Geda, Arch Gen Psychiatry 2008) 2015 MFMER slide-4

5 Population-based indices of depression Author Study Sample size/age Prevalence/Frequency Lyketsos et al., 2002 Geda et al., 2008 Lyketsos et al., 2000 Steffens et al., 2000 Okura et al., 2010 Chan et al., 2003 Luppa et al., 2011 Cardiovascular Health Study Mayo Clinic Study of Aging 320 MCI, 362 dementia, 65 yrs 329 MCI, 1640 CN, 70 yrs Cache County Study 673 no dementia, 329 dementia, 65 yrs Cache County Study Aging, Demographics & Memory Study Memory and Medical Care Study, MD, USA Leipzig Study of the Aged, GER 4559 no dementia, 65 yrs 20.1% (MCI), 32.3% (dementia) 27.0% (MCI), 11.4% (CN) 7.0% (CN), 23.7% (dementia) Point prevalence: 5.3% Lifetime prevalence: 15.8% 856, 71 yrs 12% (CN), 30% (CIND), 25% (dementia) 121 MCI, 333 dementia 1006, 75 yrs 38.2% 15.7% (MCI), 21.9% (dementia) 2015 MFMER slide-5

6 Depression predicting CN to imci Steenland et al., 2012 (NACC) 1 Richard et al., 2013 (North Manhattan) Geda et al., 2014 (MCSA) Geda et al., 2006 (MCSA) Goveas et al., 2011 (Womens Health) Dotson et al., 2010 (BLSA) Wilson et al., 2007 Panza et al., 2008 (Italian Study on Aging) Relative Risk Hazard Ratio 2015 MFMER slide-6

7 Depression predicting MCI to idementia/ iad Rosenberg et al., 2013 (NACC) 1 Van der Mussele et al., 2014 (Belgium) 2 Pink et al., 2015 (MCSA) Goveas et al., 2011 (Womens Health) Dotson et al., 2010 (BLSA) Devanand et al., 1996 (North Manhattan) Panza et al., 2008 (Italian Study on Aging) Modrego et al., 2004 Palmer et al., Relative Risk Hazard Ratio 1 GDS > 0; 2 GDS MFMER slide-7

8 Potential mechanisms linking NPS with MCI/ dementia Etiologic pathway NPS Unknown mechanisms MCI Shared risk factor/ confounding Amyloid deposition NPS MCI Reverse causality Neuropathological changes MCI NPS Interaction Amyloid deposition Interaction MCI NPS Adapted from Geda et al., Alzheimers Dement Sep;9(5): MFMER slide-8

9 Study Setting Prospective cohort study derived from the populationbased Mayo Clinic Study of Aging in Olmsted County, MN PI: Dr. Ronald C. Petersen (Roberts, Geda et al., 2008) MN WI IA Olmsted County Rochester, MN 2015 MFMER slide-9

10 Methods Classification of normal cognitive aging, MCI, and dementia adjudicated by an expert consensus panel based on published criteria after reviewing neurologic, cognitive, and other pertinent data Hazard ratios (HR) and 95% confidence intervals (95% CI) were computed using Cox proportional hazards model, with age as a time scale NPS at baseline : measured by Neuropsychiatric Inventory Questionnaire (NPI-Q) 2015 MFMER slide-10

11 Study 1: Objective Prospective cohort study to estimate the risk of incident mild cognitive impairment (MCI) in cognitively normal elderly (aged 70 years) individuals, with or without neuropsychiatric symptoms (NPS) at baseline 2015 MFMER slide-11

12 Design: Prospective cohort study CN + NPS Incident MCI No incident MCI CN N = 1587 CN - NPS Incident MCI No incident MCI Median follow up time = 5.0 years [3.8, 5.3] 2015 MFMER slide-12

13 2015 MFMER slide-13

14 2015 MFMER slide-14

15 Conclusion HR for hippocampal volume in predicting incident MCI is 1.8 (95% CI= ) (Kantarci et al., 2013) HR for apathy in predicting incident MCI is 2.26 (95% CI= ) and 3.06 for agitation (95% CI= ) Difference in strength of predicting incident MCI by biomarker compared to NPS cannot be attributed to methodological difference (both research took place in the context of MCSA) Risk of incident MCI by baseline NPS was as strong as or stronger than risk predicted by APOEε4, medical comorbidities, or demographic variables (e.g., low education) 2015 MFMER slide-15

16 Study 2: Objective To investigate the population-based interaction between a biological variable (APOEε4), NPS, and the risk of incident dementia among subjects with prevalent MCI 2015 MFMER slide-16

17 Design: Prospective cohort study MCI + NPS N = 71 Incident dementia No incident dementia Prevalent MCI N = 275 MCI NPS N = 204 Incident dementia No incident dementia Median follow up time = 2.8 years [1.1, 4.8] 2015 MFMER slide-17

18 2015 MFMER slide-18

19 2015 MFMER slide-19

20 Interaction between NPS, APOEε4 and incident dementia 2015 MFMER slide-20

21 Conclusion NPS (depression, apathy, agitation) significantly predict progression from prevalent MCI to incident dementia Synergistic interaction between depression or apathy and APOE ε4 in further elevating the risk of incident dementia NPS may thus be useful clinical markers and clinicians may want to conduct a thorough evaluation looking for NPS If and when an NPS is identified then treatment may be warranted 2015 MFMER slide-21

22 NPS and neuroimaging biomarkers of presymptomatic AD Our team has reported cross-sectional associations between anxiety symptoms with reduced global cortical thickness and reduced thickness of the frontal and temporal cortex as measured by MRI (Pink et al., 2016) depressive and anxiety symptoms with an abnormal FDG-PET, and the point estimate is even higher for APOE ɛ4 carriers (Krell-Roesch et al., 2016) depression and anxiety with an abnormal PiB-PET (Krell- Roesch et al., in press) 2015 MFMER slide-22

23 Theoretical model linking NPS with AD biomarkers and cognitive outcomes β-amyloid Neurodegeneration NPS Cognition Incident MCI/ dementia Strong evidence Less evidence Geda et al American Journal of Geriatric Psychiatry 2015 MFMER slide-23

24 Acknowledgement Janina Krell-Roesch, PhD and members of the Geda lab at Mayo Clinic Scottsdale, AZ Colleagues and co-investigators from the Mayo Clinic Study of Aging in Rochester, MN Funding sources: NIA grants AG06786, K01 AG028573; NIMH grant K01 MH68351; National Center for Research Resources grant RR (Mayo Clinic CTSA [Career Transition Award]); RWJ Foundation (Harold Amos); Project no. LQ1605 from the National Program of Sustainability II (MEYS CR); Robert H. and Clarice Smith and Abigail Van Buren Alzheimer s Disease Research Program; Edli Foundation 2015 MFMER slide-24

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