- Email: [email protected]
ASSOCIATION OF HYPERTENSION WITH IN VIVO ALZHEIMER’S DISEASE PATHOLOGIES IN COGNITIVELY NORMAL, MCI AND DEMENTIA INDIVIDUALS
P1384
P4-264
Poster Presentations: Wednesday, July 19, 2017
underwent comprehensive clinical assessment, 11C-labelled Pittsburgh Compound B (PiB) positron emission tomography and magnetic resonance imaging. Comorbid hypertension was identified through systematic interview with subjects and their informants by trained nurses, when subjects were diagnosed with hypertension or treated for hypertension. As an Ab biomarker of AD, global cerebral Ab deposition was calculated as mean cortical PiB retention value (standardized uptake value ratio, SUVR) of the region-of-interests (ROIs) including the frontal, lateral temporal, lateral parietal and precuneus/posterior cingulate cortices. Subjects were defined to be Ab positive if they have one or more ROIs with SUVR > 1.4. As a neuronal injury biomarker of AD, AD-signature region (ADsig) cortical thickness was defined as a mean cortical thickness of the regions including the bilateral inferior and middle temporal, entorhinal cortices and fusiform gyrus. Results: In CN and MCI, hypertension was not associated with global cerebral Ab deposition and Ab positivity rate. However, the presence of hypertension was significantly associated with lower global Ab retention value and Ab positivity rate in ADD. In terms of neuronal injury biomarkers, hypertension was significantly associated with reduced ADsig cortical thickness only in CN, but not in MCI or ADD. Conclusions: Hypertension appears to contribute to the occurrence of clinical ADD by increasing neural injury or lowering brain reserve rather than by increasing cerebral Ab burden.
ASSOCIATION OF HYPERTENSION WITH IN VIVO ALZHEIMER’S DISEASE PATHOLOGIES IN COGNITIVELY NORMAL, MCI AND DEMENTIA INDIVIDUALS
So Yeon Jeon1, Min Soo Byun2, Dahyun Lee2, Jun Ho Lee1, Young Min Choe3, Kang Ko1, Seung Hoon Lee1, Na Young Han1, jee Wook Kim4, Bo Kyung Sohn5, Jun Young Lee5, Dong Young Lee6, 1 Seoul National University Hospital, Seoul, Republic of South Korea; 2 Medical Research Center Seoul National University, Seoul, Republic of South Korea; 3Ulsan University Hospital, Ulsan, Republic of South Korea; 4 Hallym University Dongtan Sacred Hospital, Seoul, Republic of South Korea; 5SMG-SNU Boramae Medical Center, Seoul, Republic of South Korea; 6Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of South Korea. Contact e-mail: [email protected] Background: Hypertension increases the risk of Alzheimer’s disease (AD) dementia. However, the relationship between hypertension and AD pathologies is still poorly understood. This study aimed to investigate the association of hypertension with in vivo AD pathologies including cerebral Ab burden and neuronal injury in cognitively normal (CN), mild cognitive impairment (MCI) and AD dementia (ADD) individuals. Methods: Twentyhundred sixty CN, 71 MCI, and 59 ADD elderly subjects from the Korean Brain Aging Study for Early Diagnosis & Prediction of Alzheimer’s Disease (KBASE) were included. All participants
Table 1 Demographic and clinical characteristics CN (n¼260)
Age, years Sex (F%) Education, years ApoE4+, N(%) Global CDR CDR-SOB Vascular risk score Vascular risk factor Antihypertensive medication use Diabetes Mellitus, N(%) Coronary artery disease, N(%) Hyperlipidemia, N(%) Stroke, N(%) TIA, N(%)
MCI (n¼71)
total
no HTN (n¼142)
HTN (n¼118)
68.768.0 133 (51.2%) 11.864.7 47 (18.1%)
67.267.9 67 (47.2%) 12.364.4 23 (16.3%)
70.567.8 66 (55.9%) 11.365.0 24 (20.3%)
1.060.9
0.460.6
1.860.7
115
0
115
p-value
total
0.001* 0.160 0.079 0.402
73.566.5 50 (70.4%) 10.464.6 29 (40.8%) 0.506.000a 1.6860.73 <0.001* 1.161.0
35
AD (n¼59) no HTN (n¼36)
HTN (n¼35)
total
no HTN (n¼36)
HTN (n¼23)
72.266.7 27 (75.0%) 10.664.5 16 (44.4%) 0.506.000a 1.760.8 0.460.6
74.866.1 0.088 23 (65.7%) 0.391 10.164.8 0.413 13 (37.1%) 0.531 0.506.000a 1.760.7 0.914 1.760.8 <0.001*
73.168.2 41 (69.5%) 9.265.7 32 (54.2%) 0.8360.24 4.9361.30 0.961.0
72.068.4 26 (72.2%) 8.865.4 19 (52.8%) 0.960.2 5.261.3 0.360.5
74.767.8 0.226 15 (65.2%) 0.569 9.866.2 0.497 13 (56.5%) 0.778 0.760.3 0.017* 4.661.3 0.083 1.860.8 <0.001*
0
35
23
0
23
p-value
p-value
46 (17.7%) 18 (12.7%) 28 (23.7%)
0.020* 14 (19.7%)
5 (13.9%)
9 (25.7%)
0.211
8 (13.6%)
3 (8.3%)
5 (21.7%)
0.142
13 (5.0%)
0.019*
0 (0%)
3 (8.6%)
0.115
4 (6.8%)
2 (5.6%)
2 (8.7%)
0.395
3 (2.1%)
10 (8.5%)
87 (33.5%) 36 (25.4%) 51 (43.2%) 0 0 0 2 (0.8%) 1 1
3 (4.2%)
0.010* 24 (33.8%) 10 (27.8%) 14 (40.0%) 0 0 0 0 0 0
0.368
18 (30.5%) 6 (16.7%) 12 (52.2%) 0 0.360.5 0 0 0.360.5 0
0.004*
Note : Data for continuous variables presented as means 6 SD. Categorical variables are presented as N (%) and analyzed through c2 test in each group. Independent t-tests were performed to compare age, education, global CDR, CDR-SOB and VRS in each diagnostic group. CN : Cognitively normal; MCI : mild cognitive impairment; AD : Alzheimer’s disease ; HTN : hypertension ; ApoE : Apolipoprotein E ; CDR SOB : Clinical Dementia Rating sum of box; TIA : Transient ischemic attack.
P4-264
Poster Presentations: Wednesday, July 19, 2017
underwent comprehensive clinical assessment, 11C-labelled Pittsburgh Compound B (PiB) positron emission tomography and magnetic resonance imaging. Comorbid hypertension was identified through systematic interview with subjects and their informants by trained nurses, when subjects were diagnosed with hypertension or treated for hypertension. As an Ab biomarker of AD, global cerebral Ab deposition was calculated as mean cortical PiB retention value (standardized uptake value ratio, SUVR) of the region-of-interests (ROIs) including the frontal, lateral temporal, lateral parietal and precuneus/posterior cingulate cortices. Subjects were defined to be Ab positive if they have one or more ROIs with SUVR > 1.4. As a neuronal injury biomarker of AD, AD-signature region (ADsig) cortical thickness was defined as a mean cortical thickness of the regions including the bilateral inferior and middle temporal, entorhinal cortices and fusiform gyrus. Results: In CN and MCI, hypertension was not associated with global cerebral Ab deposition and Ab positivity rate. However, the presence of hypertension was significantly associated with lower global Ab retention value and Ab positivity rate in ADD. In terms of neuronal injury biomarkers, hypertension was significantly associated with reduced ADsig cortical thickness only in CN, but not in MCI or ADD. Conclusions: Hypertension appears to contribute to the occurrence of clinical ADD by increasing neural injury or lowering brain reserve rather than by increasing cerebral Ab burden.
ASSOCIATION OF HYPERTENSION WITH IN VIVO ALZHEIMER’S DISEASE PATHOLOGIES IN COGNITIVELY NORMAL, MCI AND DEMENTIA INDIVIDUALS
So Yeon Jeon1, Min Soo Byun2, Dahyun Lee2, Jun Ho Lee1, Young Min Choe3, Kang Ko1, Seung Hoon Lee1, Na Young Han1, jee Wook Kim4, Bo Kyung Sohn5, Jun Young Lee5, Dong Young Lee6, 1 Seoul National University Hospital, Seoul, Republic of South Korea; 2 Medical Research Center Seoul National University, Seoul, Republic of South Korea; 3Ulsan University Hospital, Ulsan, Republic of South Korea; 4 Hallym University Dongtan Sacred Hospital, Seoul, Republic of South Korea; 5SMG-SNU Boramae Medical Center, Seoul, Republic of South Korea; 6Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of South Korea. Contact e-mail: [email protected] Background: Hypertension increases the risk of Alzheimer’s disease (AD) dementia. However, the relationship between hypertension and AD pathologies is still poorly understood. This study aimed to investigate the association of hypertension with in vivo AD pathologies including cerebral Ab burden and neuronal injury in cognitively normal (CN), mild cognitive impairment (MCI) and AD dementia (ADD) individuals. Methods: Twentyhundred sixty CN, 71 MCI, and 59 ADD elderly subjects from the Korean Brain Aging Study for Early Diagnosis & Prediction of Alzheimer’s Disease (KBASE) were included. All participants
Table 1 Demographic and clinical characteristics CN (n¼260)
Age, years Sex (F%) Education, years ApoE4+, N(%) Global CDR CDR-SOB Vascular risk score Vascular risk factor Antihypertensive medication use Diabetes Mellitus, N(%) Coronary artery disease, N(%) Hyperlipidemia, N(%) Stroke, N(%) TIA, N(%)
MCI (n¼71)
total
no HTN (n¼142)
HTN (n¼118)
68.768.0 133 (51.2%) 11.864.7 47 (18.1%)
67.267.9 67 (47.2%) 12.364.4 23 (16.3%)
70.567.8 66 (55.9%) 11.365.0 24 (20.3%)
1.060.9
0.460.6
1.860.7
115
0
115
p-value
total
0.001* 0.160 0.079 0.402
73.566.5 50 (70.4%) 10.464.6 29 (40.8%) 0.506.000a 1.6860.73 <0.001* 1.161.0
35
AD (n¼59) no HTN (n¼36)
HTN (n¼35)
total
no HTN (n¼36)
HTN (n¼23)
72.266.7 27 (75.0%) 10.664.5 16 (44.4%) 0.506.000a 1.760.8 0.460.6
74.866.1 0.088 23 (65.7%) 0.391 10.164.8 0.413 13 (37.1%) 0.531 0.506.000a 1.760.7 0.914 1.760.8 <0.001*
73.168.2 41 (69.5%) 9.265.7 32 (54.2%) 0.8360.24 4.9361.30 0.961.0
72.068.4 26 (72.2%) 8.865.4 19 (52.8%) 0.960.2 5.261.3 0.360.5
74.767.8 0.226 15 (65.2%) 0.569 9.866.2 0.497 13 (56.5%) 0.778 0.760.3 0.017* 4.661.3 0.083 1.860.8 <0.001*
0
35
23
0
23
p-value
p-value
46 (17.7%) 18 (12.7%) 28 (23.7%)
0.020* 14 (19.7%)
5 (13.9%)
9 (25.7%)
0.211
8 (13.6%)
3 (8.3%)
5 (21.7%)
0.142
13 (5.0%)
0.019*
0 (0%)
3 (8.6%)
0.115
4 (6.8%)
2 (5.6%)
2 (8.7%)
0.395
3 (2.1%)
10 (8.5%)
87 (33.5%) 36 (25.4%) 51 (43.2%) 0 0 0 2 (0.8%) 1 1
3 (4.2%)
0.010* 24 (33.8%) 10 (27.8%) 14 (40.0%) 0 0 0 0 0 0
0.368
18 (30.5%) 6 (16.7%) 12 (52.2%) 0 0.360.5 0 0 0.360.5 0
0.004*
Note : Data for continuous variables presented as means 6 SD. Categorical variables are presented as N (%) and analyzed through c2 test in each group. Independent t-tests were performed to compare age, education, global CDR, CDR-SOB and VRS in each diagnostic group. CN : Cognitively normal; MCI : mild cognitive impairment; AD : Alzheimer’s disease ; HTN : hypertension ; ApoE : Apolipoprotein E ; CDR SOB : Clinical Dementia Rating sum of box; TIA : Transient ischemic attack.