- Email: [email protected]
GAIT AND COGNITION SYNDROME AND RISK OF DEMENTIA IN THE GAIT AND BRAIN STUDY
Podium Presentations: Monday, July 17, 2017
education groups. The group with lower education was less frequently amyloid positive (23% vs. 60%) but had more instances of impaired cognition (44% vs. 27%). Nominal logistic regression for amyloid negative group revealed the odds of impaired cognition in those without a college degree was not significantly different compared to the group with higher education (OR: 3.5, 95% CI: 0.7-25.7, p¼0.14). However, logistic regression analysis of amyloid positive individuals showed those without a college degree had a 32-fold increase in the odds of impaired cognition (OR 32.1, 95% CI: 4.6-419.6, p<0.01) compared to those with a college degree or more. Conclusions: The findings of our study imply higher education might render oldest old individuals with abnormal amyloid levels resilient to cognitive decline. The double dissociation of amyloid positivity and impaired cognition frequency makes the above results even more compelling.
O2-10-02
GAIT AND COGNITION SYNDROME AND RISK OF DEMENTIA IN THE GAIT AND BRAIN STUDY
Manuel Montero-Odasso1, Yanina Sarquis-Adamson1, Mark Speechley1, Susan Muir-Hunter1, Luciano Sposato1, Jennie Wells1, Michael Borrie1, Richard Camicioli2, 1Parkwood Institute, London, ON, Canada; 2University of Alberta, Edmonton, AB, Canada. Contact e-mail: manuel.monteroodasso@sjhc. london.on.ca Background: Combining objective cognitive impairment with slow
gait to predict future dementia remains to be explored. We examined whether the combination of objective low cognitive performance and slow gait velocity, defined as “Gait and Cognition syndrome” is a better predictor of incident dementia than low cognition or slow gait velocity alone. Methods: Cohort study of 298 community older adults free of dementia at baseline with a 5 year follow-up and biannual assessments. Global cognition was assessed using the MoCA, and gait velocity (cm/s) using an electronic walkway. “Gait and Cognition syndrome” was operationalized as the simultaneous presence of slow gait (<1 m/s) and low baseline MoCA (<26), and absence of dementia. Main outcome was allcause dementia (DSM-IV criteria). Cox Proportional Hazards models were used to estimate the risk of incident dementia when participants had a) slow gait (“pure slow gait”), b) low MoCA (“pure cognitive impairment”), and c) slow gait and low MoCA (“Gait and Cognition syndrome”). Results: Over a 5-year followup, 53 participants experienced cognitive decline and 29 progressed to dementia (incidence rate [IR]:73/1000-person/y). Pure slow gait and pure cognitive impairment posed risks for progression to dementia of HR: 1.2 (95%CI:0.2-5.9; p ¼0.860) and HR: 1.5 (95% CI:0.6-4.0; p¼0.377), respectively. The Gait and Cognition syndrome showed the highest risk for progression to dementia (HR: 5.1, 95%CI:1.1–14.8; p¼0.003) with an IR of 130/1000 person/y. Conclusions: Combining a simple objective mobility measure, such as gait velocity, with a reliable cognitive test like MoCA is superior than pure slow gait or pure objective cognitive impairment to detect high-risk individuals for progression to dementia syndromes. This can serve as screening strategies for detecting older adult at high risk of dementia.
O2-10-03
P577
SEVERITY OF SUBJECTIVE COGNITIVE DECLINE ALIGNS WITH REGIONAL AMYLOID SEVERITY: FINDINGS FROM THE HARVARD AGING BRAIN STUDY
Rachel F. Buckley1,2,3, Bernard J. Hanseeuw4, Aaron P. Schultz5,6, Patrizia Vannini1,6,7,8,9, Jonathan D. Jackson10, Kate V. Papp4,6,9,11, Beth C. Mormino4,12, Dorene M. Rentz1,6,9,11, Reisa A. Sperling6,7,9,11,13,14, Keith Johnson1,7,8,15,16, Rebecca Amariglio6,9,10,11, 1Massachusetts General Hospital, Charlestown, MA, USA; 2University of Melbourne, Melbourne, Australia; 3The Florey Institute of Neuroscience and Mental Health, Melbourne, Australia; 4Massachusetts General Hospital, Boston, MA, USA; 5 Massachusetts General Hospital, Athinoula A. Martinos Center for Biomedical Imaging, Harvard Medical School, Boston, MA, USA; 6Harvard Medical School, Boston, MA, USA; 7Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA; 8Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA; 9Brigham and Women’s Hospital, Boston, MA, USA; 10Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA; 11Center for Alzheimer Research and Treatment, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA; 12Stanford University School of Medicine, Palo Alto, CA, USA; 13Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; 14Massachusetts General Hospital and the Athinoula A Martinos Center for Biomedical Imaging, Boston, MA, USA; 15Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; 16Department of Radiology, Division of Molecular Imaging and Nuclear Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Contact e-mail: [email protected] Background: Post-mortem and neuroimaging studies suggest that
striatal Ab is a useful predictor of Alzheimer’s disease clinicopathology, and later Braak neurofibrillary tangle stages. Striatal Ab deposition appears after neocortical Ab deposition, with evidence of both predicting the steepest cognitive decline in clinicallynormal older adults (Hanseeuw, submitted 2017). Subjective cognitive decline (SCD) is associated with neocortical Ab, but studies have not examined neocortical Ab and striatal Ab simultaneously. We examined the hypothesis that neocortical Ab, followed by neocortical and striatal Ab, would incrementally influence SCD severity. Methods: 286 older participants (74yrs, SD¼6.4, CDR 0¼281/CDR 0.5¼5) from the Harvard Aging Brain Study underwent PiB-PET imaging and neuropsychological assessment. Striatal Ab was an average of caudate and putamen ROIs, with a cut-off>1.64 distribution value ratio as derived using Gaussian mixture modeling. Neocortical Ab was a composite measure of frontal, lateral and retrosplenial tracer (FLR) uptake. An Ab group was created to emulate three stages of increasing amyloidosis severity; Ab FLR- (n¼207); Ab FLR+/striatal Ab- (n¼42); Ab FLR+/striatal Ab+ (n¼37). The Ab FLR- group was not stratified by striatal Ab, as only two participants exhibited high striatal Ab burden with low Ab FLR. An SCD composite was created using z- transformed subscales from three measures; the Memory Functioning Questionnaire (MFQ), the Everyday Cognition (ECog) battery and a seven-item concern measure. Results: Greater SCD was correlated with greater continuous striatal Ab, r(284)¼0.22, p¼.0002 (A), and also greater Ab FLR, r(284)¼.23, p¼.0001. SCD severity differed across the Ab groups, Kruskal-Wallis c2(2)¼14.6, p¼.0006 (B), with the most severe SCD endorsed in the Ab FLR+/striatal Ab+ group in comparison with Ab FLR-, p¼.0004 and Ab FLR+/striatal Ab-, p¼.02. Multinomial logistic
education groups. The group with lower education was less frequently amyloid positive (23% vs. 60%) but had more instances of impaired cognition (44% vs. 27%). Nominal logistic regression for amyloid negative group revealed the odds of impaired cognition in those without a college degree was not significantly different compared to the group with higher education (OR: 3.5, 95% CI: 0.7-25.7, p¼0.14). However, logistic regression analysis of amyloid positive individuals showed those without a college degree had a 32-fold increase in the odds of impaired cognition (OR 32.1, 95% CI: 4.6-419.6, p<0.01) compared to those with a college degree or more. Conclusions: The findings of our study imply higher education might render oldest old individuals with abnormal amyloid levels resilient to cognitive decline. The double dissociation of amyloid positivity and impaired cognition frequency makes the above results even more compelling.
O2-10-02
GAIT AND COGNITION SYNDROME AND RISK OF DEMENTIA IN THE GAIT AND BRAIN STUDY
Manuel Montero-Odasso1, Yanina Sarquis-Adamson1, Mark Speechley1, Susan Muir-Hunter1, Luciano Sposato1, Jennie Wells1, Michael Borrie1, Richard Camicioli2, 1Parkwood Institute, London, ON, Canada; 2University of Alberta, Edmonton, AB, Canada. Contact e-mail: manuel.monteroodasso@sjhc. london.on.ca Background: Combining objective cognitive impairment with slow
gait to predict future dementia remains to be explored. We examined whether the combination of objective low cognitive performance and slow gait velocity, defined as “Gait and Cognition syndrome” is a better predictor of incident dementia than low cognition or slow gait velocity alone. Methods: Cohort study of 298 community older adults free of dementia at baseline with a 5 year follow-up and biannual assessments. Global cognition was assessed using the MoCA, and gait velocity (cm/s) using an electronic walkway. “Gait and Cognition syndrome” was operationalized as the simultaneous presence of slow gait (<1 m/s) and low baseline MoCA (<26), and absence of dementia. Main outcome was allcause dementia (DSM-IV criteria). Cox Proportional Hazards models were used to estimate the risk of incident dementia when participants had a) slow gait (“pure slow gait”), b) low MoCA (“pure cognitive impairment”), and c) slow gait and low MoCA (“Gait and Cognition syndrome”). Results: Over a 5-year followup, 53 participants experienced cognitive decline and 29 progressed to dementia (incidence rate [IR]:73/1000-person/y). Pure slow gait and pure cognitive impairment posed risks for progression to dementia of HR: 1.2 (95%CI:0.2-5.9; p ¼0.860) and HR: 1.5 (95% CI:0.6-4.0; p¼0.377), respectively. The Gait and Cognition syndrome showed the highest risk for progression to dementia (HR: 5.1, 95%CI:1.1–14.8; p¼0.003) with an IR of 130/1000 person/y. Conclusions: Combining a simple objective mobility measure, such as gait velocity, with a reliable cognitive test like MoCA is superior than pure slow gait or pure objective cognitive impairment to detect high-risk individuals for progression to dementia syndromes. This can serve as screening strategies for detecting older adult at high risk of dementia.
O2-10-03
P577
SEVERITY OF SUBJECTIVE COGNITIVE DECLINE ALIGNS WITH REGIONAL AMYLOID SEVERITY: FINDINGS FROM THE HARVARD AGING BRAIN STUDY
Rachel F. Buckley1,2,3, Bernard J. Hanseeuw4, Aaron P. Schultz5,6, Patrizia Vannini1,6,7,8,9, Jonathan D. Jackson10, Kate V. Papp4,6,9,11, Beth C. Mormino4,12, Dorene M. Rentz1,6,9,11, Reisa A. Sperling6,7,9,11,13,14, Keith Johnson1,7,8,15,16, Rebecca Amariglio6,9,10,11, 1Massachusetts General Hospital, Charlestown, MA, USA; 2University of Melbourne, Melbourne, Australia; 3The Florey Institute of Neuroscience and Mental Health, Melbourne, Australia; 4Massachusetts General Hospital, Boston, MA, USA; 5 Massachusetts General Hospital, Athinoula A. Martinos Center for Biomedical Imaging, Harvard Medical School, Boston, MA, USA; 6Harvard Medical School, Boston, MA, USA; 7Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA; 8Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA; 9Brigham and Women’s Hospital, Boston, MA, USA; 10Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA; 11Center for Alzheimer Research and Treatment, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA; 12Stanford University School of Medicine, Palo Alto, CA, USA; 13Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; 14Massachusetts General Hospital and the Athinoula A Martinos Center for Biomedical Imaging, Boston, MA, USA; 15Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; 16Department of Radiology, Division of Molecular Imaging and Nuclear Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Contact e-mail: [email protected] Background: Post-mortem and neuroimaging studies suggest that
striatal Ab is a useful predictor of Alzheimer’s disease clinicopathology, and later Braak neurofibrillary tangle stages. Striatal Ab deposition appears after neocortical Ab deposition, with evidence of both predicting the steepest cognitive decline in clinicallynormal older adults (Hanseeuw, submitted 2017). Subjective cognitive decline (SCD) is associated with neocortical Ab, but studies have not examined neocortical Ab and striatal Ab simultaneously. We examined the hypothesis that neocortical Ab, followed by neocortical and striatal Ab, would incrementally influence SCD severity. Methods: 286 older participants (74yrs, SD¼6.4, CDR 0¼281/CDR 0.5¼5) from the Harvard Aging Brain Study underwent PiB-PET imaging and neuropsychological assessment. Striatal Ab was an average of caudate and putamen ROIs, with a cut-off>1.64 distribution value ratio as derived using Gaussian mixture modeling. Neocortical Ab was a composite measure of frontal, lateral and retrosplenial tracer (FLR) uptake. An Ab group was created to emulate three stages of increasing amyloidosis severity; Ab FLR- (n¼207); Ab FLR+/striatal Ab- (n¼42); Ab FLR+/striatal Ab+ (n¼37). The Ab FLR- group was not stratified by striatal Ab, as only two participants exhibited high striatal Ab burden with low Ab FLR. An SCD composite was created using z- transformed subscales from three measures; the Memory Functioning Questionnaire (MFQ), the Everyday Cognition (ECog) battery and a seven-item concern measure. Results: Greater SCD was correlated with greater continuous striatal Ab, r(284)¼0.22, p¼.0002 (A), and also greater Ab FLR, r(284)¼.23, p¼.0001. SCD severity differed across the Ab groups, Kruskal-Wallis c2(2)¼14.6, p¼.0006 (B), with the most severe SCD endorsed in the Ab FLR+/striatal Ab+ group in comparison with Ab FLR-, p¼.0004 and Ab FLR+/striatal Ab-, p¼.02. Multinomial logistic