- Email: [email protected]
Cerebral amyloid deposition itself is not related to depressive symptoms in elderly individuals with normal cognition, MCI, and Alzheimer's disease
Poster Presentations: P4
P781
Sample size of different outcome markers in subjects with normal cognition
CSF ab 1-42 (pg/ml) CSF tau (pg/ml) AV-45 PET FDG PET (SUVr) Whole brain volume (cm3) Hippocampal volume (mm3) Ventricular volume (cm3) CDR sum of boxes MMSE score ADAS-Cog
Cognitively normal (n¼522)
Preclinical AD (N¼146)
Preclinical AD stage 1 (N¼110)
1490 (1031-2340) 1763 (1181-2909) 3366 (1973-6992) 3234 (2764-3837) 375 (338-419) 445 (401-498) 382 (345-425) 22882 (17987-30087) 31932 (15964-93077) -
1382 (787-3035) 744 (470-1351) 3309 (1861-7445) 209 (178-247) 345 (287-423) 333 (274-414) 1157 (880-1589) 6950 (3676-17792) -
-
Preclinical AD stage 2 (N¼34) 564 (309-1337)
961 (564-2196) 556 (368-934) 2118 (1191-4765) 278 (225-353) 635 (472-897) 400 (310-537) 1816 (1223-2972) -
106 (88-131) 100 (84-122) 236 (178-327) 1094 (671-2089) -
Abbrevations: AD, Alzheimer᾿s Disease; CSF, cerebrospinal fluid; ab 1-42 , amyloid beta 1-42; AV-45, Florbetapir, PET, Positron Emission Tomography; FDG, fluorodeoxyglucose; CDR, Clinical Dementia Rating scale; MMSE, Mini Mental State Examination; ADAS-Cog, Alzheimer᾿s Disease Assessment Scale-Cognitive. -, not significant. Data are mean (SD).
stage-1 (CN or MCI and CSF aß1-42 <192 pg/ml and CSF tau< 92 pg/ml or Florbetapir-PET >1.11 and FDG-PET>1.21). 4. Preclinical or Prodromal-AD stage-2 (CN or MCI and CSF aß1-42 <192 pg/ml and CSF tau> 92 pg/ml or Florbetapir-PET >1.11 and FDGPET<1.21). Study outcome markers were CSF aß1-42, CSF tau, Florbetapir and FDG uptake on PET, whole brain, Hippocampal, and ventricular volume on MRI, CDR-sum-of-boxes, MMSE and ADAS-Cog. For every set of inclusion criteria we estimated slopes of decline of the outcome markers, using mixed models. Sample size was calculated for the outcome markers that changed significantly over time (p<0.05). For our power calculation we assumed a fictive 3-year trial with a decline of 25%, a power of 80%, a 2sided alpha of 5% and allowed an annual dropout of 10%. Results: Of the 522 asymptomatic subjects 146 subjects had preclinical-AD, 110 had preclinical-AD stage-1 and 34 had preclinical-AD stage-2. Of the 872 MCI subjects 420 were subjects with prodromal-AD, 221 had prodromal-AD stage-1, and 198 subjects were prodromal-AD stage-2. Sample sizes for each significant outcome measure are summarized in the table. Conclusions: AD clinical trials in non-demented subjects benefit, apart from cognition, most from inclusion based on abnormal amyloid and abnormal injury markers. Inclusion based on amyloid is preferable over inclusion based on cognitive assessment alone. CSF and PET measures are equally useful for inclusion. Changes in MRI markers are most useful outcome markers, at least for proof of concept.
and depressive symptoms in elderly individuals with normal cognition (NC), amnestic mild cognitive impairment (MCI) and Alzheimer’s disease dementia (AD). Methods: Twenty-six NC, 23 MCI and 27 AD individuals were recruited. Subjects with history of major depressive episode or stroke were excluded. All subjects received three-dimensional volumetric 3T MRI, Pittsburgh Compound B (PiB)-positron emission tomography (PET) and comprehensive clinical evaluation including vascular burden assessment. Depressive symptoms were measured using Geriatric Depression Scale (GDS) and Hamilton Depression Rating Scale (HAM-D). Results: There were significant group differences of GDS and HAM-D scores among diagnostic groups, and post-hoc tests showed that AD had significantly higher GDS and HAM-D scores than NC (see Table). However, multiple linear regression analysis controlling for age, gender, diagnostic group, and vascular burden did not reveal that global cerebral Ab burden measured by PiBPET was associated with GDS or HAM-D scores. In subgroup analyses for each diagnostic group, we did not find any significant associations between global cerebral Ab burden and GDS or HAM-D scores after controlling age, gender, and vascular burden. Conclusions: Our results did not support “amyloid depression hypothesis”, while the relationship between diagnostic group and depression scores implied that late-life depression might be associated with overall brain degeneration.
P4-042 P4-041
CEREBRAL AMYLOID DEPOSITION ITSELF IS NOT RELATED TO DEPRESSIVE SYMPTOMS IN ELDERLY INDIVIDUALS WITH NORMAL COGNITION, MCI, AND ALZHEIMER’S DISEASE
Young Min Choe1, Min Soo Byun1, Dahyun Yi1, Hyo Jung Choi1, Hyewon Baek1, Bo Kyung Sohn2, Eun Hyun Seo3, Yu Kyeong Kim2, Jong Inn Woo1, Dong Young Lee1, 1Seoul National University Hospital, Seoul, South Korea; 2SMG-SNU Boramae Medical Center, Seoul, South Korea; 3Chosun University, Gwangju, South Korea. Contact e-mail: [email protected] Background: A couple of population studies demonstrated that elderly with depression have lower plasma amyloid-b 42 (Ab42) than those without depression, and so called “amyloid depression hypothesis” (i.e., the hypothesis that cerebral amyloid deposition is related to late-life depression) was proposed. This study aimed to investigate the relationship between global cerebral Ab burden
DEMENTIA WITH LEWY BODIES MANIFESTED AS DELUSIONAL PARASITOSIS (EKBOM’S SYNDROME)
Radoslaw Magierski, Joanna Magierska, Iwona Kloszewska, Tomasz Sobow, Medical University of Lodz, Lodz, Poland. Contact e-mail: [email protected] Background: Dementia with Lewy Bodies (DLB) is a dementing disease that manifests with a range of neurological and psychiatric features. Visual hallucinations, atypical parkinsonism and fluctuations of cognition are main clinical symptoms needed for diagnosis. Presentation with well-formed, constant and systematized delusions is possible and described within clinical criteria but such clinical picture is quite rare. Methods: We report two female elderly DLB cases that developed symptoms of severe delusional parasitosis (Ekbom’s syndrome) with totally disrupted everyday activity due to delusional thinking. Results: Acute onset of psychosis was a cause of psychiatric consultation in both cases and the diagnosis
P781
Sample size of different outcome markers in subjects with normal cognition
CSF ab 1-42 (pg/ml) CSF tau (pg/ml) AV-45 PET FDG PET (SUVr) Whole brain volume (cm3) Hippocampal volume (mm3) Ventricular volume (cm3) CDR sum of boxes MMSE score ADAS-Cog
Cognitively normal (n¼522)
Preclinical AD (N¼146)
Preclinical AD stage 1 (N¼110)
1490 (1031-2340) 1763 (1181-2909) 3366 (1973-6992) 3234 (2764-3837) 375 (338-419) 445 (401-498) 382 (345-425) 22882 (17987-30087) 31932 (15964-93077) -
1382 (787-3035) 744 (470-1351) 3309 (1861-7445) 209 (178-247) 345 (287-423) 333 (274-414) 1157 (880-1589) 6950 (3676-17792) -
-
Preclinical AD stage 2 (N¼34) 564 (309-1337)
961 (564-2196) 556 (368-934) 2118 (1191-4765) 278 (225-353) 635 (472-897) 400 (310-537) 1816 (1223-2972) -
106 (88-131) 100 (84-122) 236 (178-327) 1094 (671-2089) -
Abbrevations: AD, Alzheimer᾿s Disease; CSF, cerebrospinal fluid; ab 1-42 , amyloid beta 1-42; AV-45, Florbetapir, PET, Positron Emission Tomography; FDG, fluorodeoxyglucose; CDR, Clinical Dementia Rating scale; MMSE, Mini Mental State Examination; ADAS-Cog, Alzheimer᾿s Disease Assessment Scale-Cognitive. -, not significant. Data are mean (SD).
stage-1 (CN or MCI and CSF aß1-42 <192 pg/ml and CSF tau< 92 pg/ml or Florbetapir-PET >1.11 and FDG-PET>1.21). 4. Preclinical or Prodromal-AD stage-2 (CN or MCI and CSF aß1-42 <192 pg/ml and CSF tau> 92 pg/ml or Florbetapir-PET >1.11 and FDGPET<1.21). Study outcome markers were CSF aß1-42, CSF tau, Florbetapir and FDG uptake on PET, whole brain, Hippocampal, and ventricular volume on MRI, CDR-sum-of-boxes, MMSE and ADAS-Cog. For every set of inclusion criteria we estimated slopes of decline of the outcome markers, using mixed models. Sample size was calculated for the outcome markers that changed significantly over time (p<0.05). For our power calculation we assumed a fictive 3-year trial with a decline of 25%, a power of 80%, a 2sided alpha of 5% and allowed an annual dropout of 10%. Results: Of the 522 asymptomatic subjects 146 subjects had preclinical-AD, 110 had preclinical-AD stage-1 and 34 had preclinical-AD stage-2. Of the 872 MCI subjects 420 were subjects with prodromal-AD, 221 had prodromal-AD stage-1, and 198 subjects were prodromal-AD stage-2. Sample sizes for each significant outcome measure are summarized in the table. Conclusions: AD clinical trials in non-demented subjects benefit, apart from cognition, most from inclusion based on abnormal amyloid and abnormal injury markers. Inclusion based on amyloid is preferable over inclusion based on cognitive assessment alone. CSF and PET measures are equally useful for inclusion. Changes in MRI markers are most useful outcome markers, at least for proof of concept.
and depressive symptoms in elderly individuals with normal cognition (NC), amnestic mild cognitive impairment (MCI) and Alzheimer’s disease dementia (AD). Methods: Twenty-six NC, 23 MCI and 27 AD individuals were recruited. Subjects with history of major depressive episode or stroke were excluded. All subjects received three-dimensional volumetric 3T MRI, Pittsburgh Compound B (PiB)-positron emission tomography (PET) and comprehensive clinical evaluation including vascular burden assessment. Depressive symptoms were measured using Geriatric Depression Scale (GDS) and Hamilton Depression Rating Scale (HAM-D). Results: There were significant group differences of GDS and HAM-D scores among diagnostic groups, and post-hoc tests showed that AD had significantly higher GDS and HAM-D scores than NC (see Table). However, multiple linear regression analysis controlling for age, gender, diagnostic group, and vascular burden did not reveal that global cerebral Ab burden measured by PiBPET was associated with GDS or HAM-D scores. In subgroup analyses for each diagnostic group, we did not find any significant associations between global cerebral Ab burden and GDS or HAM-D scores after controlling age, gender, and vascular burden. Conclusions: Our results did not support “amyloid depression hypothesis”, while the relationship between diagnostic group and depression scores implied that late-life depression might be associated with overall brain degeneration.
P4-042 P4-041
CEREBRAL AMYLOID DEPOSITION ITSELF IS NOT RELATED TO DEPRESSIVE SYMPTOMS IN ELDERLY INDIVIDUALS WITH NORMAL COGNITION, MCI, AND ALZHEIMER’S DISEASE
Young Min Choe1, Min Soo Byun1, Dahyun Yi1, Hyo Jung Choi1, Hyewon Baek1, Bo Kyung Sohn2, Eun Hyun Seo3, Yu Kyeong Kim2, Jong Inn Woo1, Dong Young Lee1, 1Seoul National University Hospital, Seoul, South Korea; 2SMG-SNU Boramae Medical Center, Seoul, South Korea; 3Chosun University, Gwangju, South Korea. Contact e-mail: [email protected] Background: A couple of population studies demonstrated that elderly with depression have lower plasma amyloid-b 42 (Ab42) than those without depression, and so called “amyloid depression hypothesis” (i.e., the hypothesis that cerebral amyloid deposition is related to late-life depression) was proposed. This study aimed to investigate the relationship between global cerebral Ab burden
DEMENTIA WITH LEWY BODIES MANIFESTED AS DELUSIONAL PARASITOSIS (EKBOM’S SYNDROME)
Radoslaw Magierski, Joanna Magierska, Iwona Kloszewska, Tomasz Sobow, Medical University of Lodz, Lodz, Poland. Contact e-mail: [email protected] Background: Dementia with Lewy Bodies (DLB) is a dementing disease that manifests with a range of neurological and psychiatric features. Visual hallucinations, atypical parkinsonism and fluctuations of cognition are main clinical symptoms needed for diagnosis. Presentation with well-formed, constant and systematized delusions is possible and described within clinical criteria but such clinical picture is quite rare. Methods: We report two female elderly DLB cases that developed symptoms of severe delusional parasitosis (Ekbom’s syndrome) with totally disrupted everyday activity due to delusional thinking. Results: Acute onset of psychosis was a cause of psychiatric consultation in both cases and the diagnosis