- Email: [email protected]
DIETARY INFLAMMATORY INDEX, INFLAMMATION AND COGNITIVE DECLINE IN OLDER ADULTS: THE HEALTH ABC STUDY
P514
Poster Presentations: Sunday, July 16, 2017
participants with lower SDNN scored 1.76 points worse on DSST (p¼0.01) and 1.14 points worse on Stroop (p¼0.02). After adjusting for behavioral and cardiovascular risk factors, lower SDNN remained significantly associated with worse stroop (p¼0.01) but not with DSST. There was no association between RMSSD and cognitive function. Conclusions: Our findings suggest that lower SDDN is associated with worse executive function among middle-aged adults, above and beyond cardiovascular risk factors. P1-572
LONG-TERM EFFECTS OF PREDIABETES AND DIABETES ON COGNITIVE TRAJECTORIES IN A POPULATIONBASED COHORT
Anna Marseglia1, Anna K. Dahl Aslan2,3, Laura Fratiglioni3,4, Giola Santoni5, Nancy L. Pedersen3,6, Weili Xu3,7, 1Aging Research Center, Karolinska Institutet, Stockholm, Sweden; 2Jonkoping University, Jonkoping, Sweden; 3Karolinska Institutet, Stockholm, Sweden; 4Stockholm Gerontology Research Center, Stockholm, Sweden; 5Karolinska Institute, Stockholm, Sweden; 6University of Southern California, Los Angeles, CA, USA; 7Tianjin Medical University, Tianjin, China. Contact e-mail: anna. [email protected] Background: Although diabetes has been linked to dementia risk,
the cognitive trajectories in older adults with diabetes remain unclear. We aimed to investigate the effect of prediabetes and diabetes on cognitive trajectories among cognitively intact older adults in a long-term follow-up study. Methods: Within the Swedish Adoption/ Twin Study of Aging, 793 cognitively intact older adults aged 50 were identified at baseline and followed for up to 23 years. Cognitive domains (verbal, spatial/fluid, memory, perceptual speed) were assessed at baseline and up to seven follow-ups. Prediabetes was defined according to blood glucose levels in diabetes-free participants. Diabetes was ascertained based on self-report, hypoglycemic medication use and blood glucose levels. Data were analyzed with linear mixed-effect models adjusting for potential confounders. Results: At baseline, 68 participants (8.6%) had prediabetes and 45 (5.7%) had diabetes among all participants. Compared to diabetes-free individuals, people with diabetes had lower performance in spatial/fluid abilities (b -2.63; 95% CI -5.36, 0.05; p ¼ 0.058), and an accelerated linear decline over time in verbal abilities (b -0.15; 95% CI -0.29, -0.01; p ¼ 0.041). Prediabetes was associated with an accelerated decline in processing speed (b -0.01; 95% CI -0.02, -0.004; p ¼ 0.041), but with a better maintenance of memory (b 0.23; 95% CI 0.05, 0.42; p ¼ 0.013) over the follow-up. Conclusions: Prediabetes may accelerate processing speed decline, and diabetes is associated with the verbal ability decline, suggesting that diabetes and even prediabetes affect especially the cognitive domains of fluid intelligence at the early stages of cognitive impairment. P1-573
SERUM INSULIN AND THE RISK OF DEMENTIA AND COGNITIVE DECLINE: A LONGITUDINAL POPULATION-BASED STUDY
Babak Hooshmand1,2, Shireen Sindi1, Tuomo H€anninen3, Jaan Leiviska4, Hilkka Soininen5,6,7, Miia Kivipelto1,5,8,9,10, 1Karolinska Institutet, Stockholm, Sweden; 2Ulm University Hospital, Ulm, Germany; 3 Department of Neurology, Kuopio University Hospital, Kuopio, Finland; 4 National Institute for Health and Welfare (THL), Helsinki, Finland; 5 University of Eastern Finland, Kuopio, Finland; 6Neurocenter, Neurology, Kuopio University Hospital, Kuopio, Finland; 7Institute of Clinical Medicine, Kuopio, Finland; 8Kuopio University Hospital, Kuopio, Finland; 9 National Institute for Health and Welfare, Helsinki, Finland; 10Karolinska Institutet-Stockholm University, Stockholm, Sweden. Contact e-mail: Babak. [email protected]
Background: Diabetes mellitus has been linked to an increased risk of dementia and Alzheimer’s disease (AD), but it is not clear if this is due to the direct effect of insulin. Our aim was to examine the association of serum insulin with the risk of incident dementia, Alzheimer disease, and cognitive decline over 7-years in a sample of Finnish community-dwelling elderly. Methods: A dementia-free sample of 304 subjects aged 65-79 years derived from the Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study was followed up for 7 years to detect incident dementia and AD. Global cognition, episodic memory, executive functioning, verbal expression, and psychomotor speed were assessed both at baseline and at follow-up. The association of serum insulin with incident dementia and cognitive decline was analyzed with multiple logistic regression and linear risk models, respectively. Results: The odds ratios (ORs) (95% confidence interval (CI)) for each increase of 1 mU/L serum insulin were 1.11 (1.01 - 1.23) for incident dementia and 1.10 (0.99 - 1.22) for incident AD after adjusting for several potential confounders including age, sex, education, follow-up time, systolic blood pressure, diastolic blood pressure, Body mass index, history of stroke, smoking status, history of diabetes, and APOEε4 status. In addition, elevated serum insulin values at baseline were related to faster decline in global cognition over 7 years: b coefficient (SE) were -0.045 (0.02); P ¼ 0.05. No associations were found for specific cognitive domains. Conclusions: Higher concentrations of insulin are related to an increased risk of dementia and cognitive decline over 7 years. P1-574
DIETARY INFLAMMATORY INDEX, INFLAMMATION AND COGNITIVE DECLINE IN OLDER ADULTS: THE HEALTH ABC STUDY
Claire T. McEvoy1, Nitin Shivappa2, James R. Hebert3, Feng Xia4, Eric Vittinghoff1, Kristine Yaffe4,5, 1University of California, San Francisco, San Francisco, CA, USA; 2University of South Carolina, Columbia, SC, USA; 3University of South Carolina, Columbia, SC, USA; 4 San Francisco VA Medical Center, San Francisco, CA, USA; 5University of California San Francisco / San Francisco VA Medical Center, San Francisco, CA, USA. Contact e-mail: [email protected] Background: Inflammation is implicated in the pathogenesis of
Alzheimer’s disease and progression of age-related neurodegeneration. Diet is known to modulate systemic inflammation. For example, fruit and vegetables have anti-inflammatory effects and saturated fat has pro-inflammatory effects. Few studies to date have investigated inflammatory dietary factors in relation to cognitive decline. The dietary Inflammatory Index (DIITM) is an empirically derived score that reflects inflammatory potential of the diet. We examined associations between DII scores, inflammatory biomarkers and longitudinal cognitive decline in the HealthABC Study. Methods: Baseline energy-adjusted DII (E-DII) scores were computed from food frequency questionnaire data on 2,429 nondemented adults, aged 74 6 2.8 (range 69.3 to 80.9) years. Higher E-DII scores indicated greater pro-inflammatory dietary potential. Inflammatory biomarkers (CRP and IL-6) also were measured at baseline. Cognitive decline was assessed using repeated Modified Mini Mental State Examination (3MS) and Digit Symbol Substitution Test (DSST) scores over a 9-year follow-up period. Linear mixed models were used to examine the association between EDII and trajectory of cognitive decline. Results: Mean E-DII was -2.39 61.70 (range -5.49 to +2.90). In multivariable models, participants in the highest E-DII tertile (more pro-inflammatory diet) had significantly increased mean CRP levels compared to the middle and
Poster Presentations: Sunday, July 16, 2017
lowest tertiles (3.13 vs 2.77 and 2.64 ug/ml) and mean IL-6 levels (2.66 vs 2.48 and 2.44 pg/ml) (PTrend ¼ 0.01 and PTrend ¼ 0.05, respectively). Over a median 9 years of follow-up (range 1.9 to 9.5 years) we found no significant association between DII and rate of cognitive decline on the 3MS (p ¼ 0.28) or DSST (p ¼ 0.16). Conclusions: In older adults, a more pro-inflammatory diet as measured using the DII, is associated with increased inflammatory biomarkers but not with rate of cognitive decline during 9 years of follow-up. P1-575
PREVALENCE OF THE APOLIPOPROTEIN E ε4 ALLELE IN AMYLOID-b POSITIVE SUBJECTS ACROSS THE SPECTRUM OF ALZHEIMER’S DISEASE
Colin Groot1,2, Niklas Mattsson3,4, Willemijn J. Jansen5, Pieter Jelle Visser6,7, Rik Ossenkoppele2,8, 1Department of Neurology j Alzheimer Center, Amsterdam, Netherlands; 2Department of Radiology and Nuclear Medicine, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, Netherlands; 3Clinical Memory Research Unit, Lund ane University Hospital, University, Lund, Sweden; 4Memory Clinic, Sk Lund, Sweden; 5Alzheimer Center Limburg, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands; 6Maastricht University, Maastricht, Netherlands; 7VU University Medical Center, Amsterdam, Netherlands; 8Alzheimer Center and Department of Neurology, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, Netherlands. Contact e-mail: [email protected] Background: The estimated prevalence of the Apolipoprotein E ε4
(APOE ε4) allele is w25-55% in mild cognitive impairment and w50-60% in clinically defined Alzheimer’s disease (AD) dementia, compared to w15-20% in the general population. However, earlier studies have included subjects without biomarker confirmation of AD pathology, and may therefore underestimate true prevalence of APOE ε4 in AD. We assessed APOE ε4 prevalence in amyloid-positive subjects only. Methods: In this cross-sectional, multicenter study, we combined cohorts from 57 centers worldwide. This yielded a total sample of 3,451 amyloid-positive subjects as assessed by cerebrospinal fluid or positron emission tomography, including 853 with a clinical diagnosis of AD dementia, 1,810 with mild cognitive impairment (prodromal AD) and 788 controls (preclinical AD). APOE ε4 prevalence was determined for
P515
Table 1 Demographic characteristics according to diagnosis Diagnosis
N Age Sex (% male) MMSE (mean) Education (mean, y) APOE ε4 (% positive)
Preclinical AD
Prodromal AD
AD dementia
788 72.6 53 28.8 13.9 51
1810 71.8 47 26.5 12.9 64
853 69.1 45 21.6 12.9 66
AD – Alzheimer’s disease, MMSE – Mini mental state examination, APOE – Apolipoprotein E.
all diagnostic groups and generalized estimating equation models were used to assess effects of age, sex and education. Results: APOE ε4 prevalence was 66% in AD dementia, 64% in prodromal AD and 51% in preclinical AD. Prevalence decreased with advancing age in preclinical (b for change in prevalence per year ¼ -0.02, p < 0.05) and prodromal AD (b: -0.03, p < 0.01), but not in AD dementia (p ¼ 0.71). There were no effects of sex or education on APOE ε4 prevalence. Conclusions: We found higher APOE ε4 prevalence in AD dementia subjects compared to previous studies. These earlier studies did not require biomarker confirmation of amyloid pathology, which likely resulted in an underestimation of true APOE ε4 prevalence. APOE ε4 accelerates the age of onset of AD dementia, as the prevalence decreased with age in preclinical and prodromal subjects. The lack of an age effect in the AD dementia group may be partly caused by atypical variants of AD (often APOE ε4 non-carriers), which are overrepresented among early onset AD dementia patients. To our knowledge, this is the first assessment of APOE ε4 carrier prevalence in an amyloid-positive population. Our results emphasize the importance of APOE ε4 for development of AD and suggest that therapies targeting APOE ε4 function may be important for disease prevention.
P1-576
A TEN-YEAR FOLLOW-UP OF ADIPOSITY INDICATORS AND DEMENTIA IN ADULTS AGE 70-YEARS AND OLDER: THE GOTHENBURG BIRTH COHORT STUDIES
Deborah R. Gustafson1,2,3, Ilse Arnoldussen4, Valter Sundh5, 8 € Kristoffer B€ackman6, Silke Kern7, Svante Ostling , Ingmar Skoog7, 4 1 Amanda Kiliaan , University of Sk€ovde, Sk€ovde, Sweden; 2University of Gothenburg, Gothenburg, Sweden; 3SUNY Downstate Medical Center, Brooklyn, NY, USA; 4Radboud University Medical Center, Nijmegen, Netherlands; 5Neuroscience and Physiology, Gothenburg, Sweden; 6 University of Gothenburg, M€olndal, Sweden; 7Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, M€olndal, Sweden; 8Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, M€olndal, Sweden. Contact e-mail: [email protected] Background: The adiposity indicators body mass index (BMI), Figure 1. Association of age with APOE ε4 prevalence according to diagnosis. This graphical representation of APOE ε4 prevalence as a function of age in amyloid-beta positive patients shows a decrease of prevalence with advancing age in preclinical AD and prodromal AD, but not in AD dementia. AD – Alzheimer’s disease, APOE – Apolipoprotein E.
waist-hip ratio (WHR), leptin and adiponectin could be useful markers of dementia as both physical and metabolic changes occur during the preclinical dementia phase. Methods: Dementia occurrence was associated with BMI, WHR, leptin and adiponectin levels in 924 Swedish elderly without dementia participating in the Gothenburg Birth Cohort studies. These adults, age 70 years and older at baseline, were followed over a 10 year period beginning in 2000, with follow-ups in 2005 and 2009. Results: Multivariate
Poster Presentations: Sunday, July 16, 2017
participants with lower SDNN scored 1.76 points worse on DSST (p¼0.01) and 1.14 points worse on Stroop (p¼0.02). After adjusting for behavioral and cardiovascular risk factors, lower SDNN remained significantly associated with worse stroop (p¼0.01) but not with DSST. There was no association between RMSSD and cognitive function. Conclusions: Our findings suggest that lower SDDN is associated with worse executive function among middle-aged adults, above and beyond cardiovascular risk factors. P1-572
LONG-TERM EFFECTS OF PREDIABETES AND DIABETES ON COGNITIVE TRAJECTORIES IN A POPULATIONBASED COHORT
Anna Marseglia1, Anna K. Dahl Aslan2,3, Laura Fratiglioni3,4, Giola Santoni5, Nancy L. Pedersen3,6, Weili Xu3,7, 1Aging Research Center, Karolinska Institutet, Stockholm, Sweden; 2Jonkoping University, Jonkoping, Sweden; 3Karolinska Institutet, Stockholm, Sweden; 4Stockholm Gerontology Research Center, Stockholm, Sweden; 5Karolinska Institute, Stockholm, Sweden; 6University of Southern California, Los Angeles, CA, USA; 7Tianjin Medical University, Tianjin, China. Contact e-mail: anna. [email protected] Background: Although diabetes has been linked to dementia risk,
the cognitive trajectories in older adults with diabetes remain unclear. We aimed to investigate the effect of prediabetes and diabetes on cognitive trajectories among cognitively intact older adults in a long-term follow-up study. Methods: Within the Swedish Adoption/ Twin Study of Aging, 793 cognitively intact older adults aged 50 were identified at baseline and followed for up to 23 years. Cognitive domains (verbal, spatial/fluid, memory, perceptual speed) were assessed at baseline and up to seven follow-ups. Prediabetes was defined according to blood glucose levels in diabetes-free participants. Diabetes was ascertained based on self-report, hypoglycemic medication use and blood glucose levels. Data were analyzed with linear mixed-effect models adjusting for potential confounders. Results: At baseline, 68 participants (8.6%) had prediabetes and 45 (5.7%) had diabetes among all participants. Compared to diabetes-free individuals, people with diabetes had lower performance in spatial/fluid abilities (b -2.63; 95% CI -5.36, 0.05; p ¼ 0.058), and an accelerated linear decline over time in verbal abilities (b -0.15; 95% CI -0.29, -0.01; p ¼ 0.041). Prediabetes was associated with an accelerated decline in processing speed (b -0.01; 95% CI -0.02, -0.004; p ¼ 0.041), but with a better maintenance of memory (b 0.23; 95% CI 0.05, 0.42; p ¼ 0.013) over the follow-up. Conclusions: Prediabetes may accelerate processing speed decline, and diabetes is associated with the verbal ability decline, suggesting that diabetes and even prediabetes affect especially the cognitive domains of fluid intelligence at the early stages of cognitive impairment. P1-573
SERUM INSULIN AND THE RISK OF DEMENTIA AND COGNITIVE DECLINE: A LONGITUDINAL POPULATION-BASED STUDY
Babak Hooshmand1,2, Shireen Sindi1, Tuomo H€anninen3, Jaan Leiviska4, Hilkka Soininen5,6,7, Miia Kivipelto1,5,8,9,10, 1Karolinska Institutet, Stockholm, Sweden; 2Ulm University Hospital, Ulm, Germany; 3 Department of Neurology, Kuopio University Hospital, Kuopio, Finland; 4 National Institute for Health and Welfare (THL), Helsinki, Finland; 5 University of Eastern Finland, Kuopio, Finland; 6Neurocenter, Neurology, Kuopio University Hospital, Kuopio, Finland; 7Institute of Clinical Medicine, Kuopio, Finland; 8Kuopio University Hospital, Kuopio, Finland; 9 National Institute for Health and Welfare, Helsinki, Finland; 10Karolinska Institutet-Stockholm University, Stockholm, Sweden. Contact e-mail: Babak. [email protected]
Background: Diabetes mellitus has been linked to an increased risk of dementia and Alzheimer’s disease (AD), but it is not clear if this is due to the direct effect of insulin. Our aim was to examine the association of serum insulin with the risk of incident dementia, Alzheimer disease, and cognitive decline over 7-years in a sample of Finnish community-dwelling elderly. Methods: A dementia-free sample of 304 subjects aged 65-79 years derived from the Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study was followed up for 7 years to detect incident dementia and AD. Global cognition, episodic memory, executive functioning, verbal expression, and psychomotor speed were assessed both at baseline and at follow-up. The association of serum insulin with incident dementia and cognitive decline was analyzed with multiple logistic regression and linear risk models, respectively. Results: The odds ratios (ORs) (95% confidence interval (CI)) for each increase of 1 mU/L serum insulin were 1.11 (1.01 - 1.23) for incident dementia and 1.10 (0.99 - 1.22) for incident AD after adjusting for several potential confounders including age, sex, education, follow-up time, systolic blood pressure, diastolic blood pressure, Body mass index, history of stroke, smoking status, history of diabetes, and APOEε4 status. In addition, elevated serum insulin values at baseline were related to faster decline in global cognition over 7 years: b coefficient (SE) were -0.045 (0.02); P ¼ 0.05. No associations were found for specific cognitive domains. Conclusions: Higher concentrations of insulin are related to an increased risk of dementia and cognitive decline over 7 years. P1-574
DIETARY INFLAMMATORY INDEX, INFLAMMATION AND COGNITIVE DECLINE IN OLDER ADULTS: THE HEALTH ABC STUDY
Claire T. McEvoy1, Nitin Shivappa2, James R. Hebert3, Feng Xia4, Eric Vittinghoff1, Kristine Yaffe4,5, 1University of California, San Francisco, San Francisco, CA, USA; 2University of South Carolina, Columbia, SC, USA; 3University of South Carolina, Columbia, SC, USA; 4 San Francisco VA Medical Center, San Francisco, CA, USA; 5University of California San Francisco / San Francisco VA Medical Center, San Francisco, CA, USA. Contact e-mail: [email protected] Background: Inflammation is implicated in the pathogenesis of
Alzheimer’s disease and progression of age-related neurodegeneration. Diet is known to modulate systemic inflammation. For example, fruit and vegetables have anti-inflammatory effects and saturated fat has pro-inflammatory effects. Few studies to date have investigated inflammatory dietary factors in relation to cognitive decline. The dietary Inflammatory Index (DIITM) is an empirically derived score that reflects inflammatory potential of the diet. We examined associations between DII scores, inflammatory biomarkers and longitudinal cognitive decline in the HealthABC Study. Methods: Baseline energy-adjusted DII (E-DII) scores were computed from food frequency questionnaire data on 2,429 nondemented adults, aged 74 6 2.8 (range 69.3 to 80.9) years. Higher E-DII scores indicated greater pro-inflammatory dietary potential. Inflammatory biomarkers (CRP and IL-6) also were measured at baseline. Cognitive decline was assessed using repeated Modified Mini Mental State Examination (3MS) and Digit Symbol Substitution Test (DSST) scores over a 9-year follow-up period. Linear mixed models were used to examine the association between EDII and trajectory of cognitive decline. Results: Mean E-DII was -2.39 61.70 (range -5.49 to +2.90). In multivariable models, participants in the highest E-DII tertile (more pro-inflammatory diet) had significantly increased mean CRP levels compared to the middle and
Poster Presentations: Sunday, July 16, 2017
lowest tertiles (3.13 vs 2.77 and 2.64 ug/ml) and mean IL-6 levels (2.66 vs 2.48 and 2.44 pg/ml) (PTrend ¼ 0.01 and PTrend ¼ 0.05, respectively). Over a median 9 years of follow-up (range 1.9 to 9.5 years) we found no significant association between DII and rate of cognitive decline on the 3MS (p ¼ 0.28) or DSST (p ¼ 0.16). Conclusions: In older adults, a more pro-inflammatory diet as measured using the DII, is associated with increased inflammatory biomarkers but not with rate of cognitive decline during 9 years of follow-up. P1-575
PREVALENCE OF THE APOLIPOPROTEIN E ε4 ALLELE IN AMYLOID-b POSITIVE SUBJECTS ACROSS THE SPECTRUM OF ALZHEIMER’S DISEASE
Colin Groot1,2, Niklas Mattsson3,4, Willemijn J. Jansen5, Pieter Jelle Visser6,7, Rik Ossenkoppele2,8, 1Department of Neurology j Alzheimer Center, Amsterdam, Netherlands; 2Department of Radiology and Nuclear Medicine, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, Netherlands; 3Clinical Memory Research Unit, Lund ane University Hospital, University, Lund, Sweden; 4Memory Clinic, Sk Lund, Sweden; 5Alzheimer Center Limburg, School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands; 6Maastricht University, Maastricht, Netherlands; 7VU University Medical Center, Amsterdam, Netherlands; 8Alzheimer Center and Department of Neurology, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, Netherlands. Contact e-mail: [email protected] Background: The estimated prevalence of the Apolipoprotein E ε4
(APOE ε4) allele is w25-55% in mild cognitive impairment and w50-60% in clinically defined Alzheimer’s disease (AD) dementia, compared to w15-20% in the general population. However, earlier studies have included subjects without biomarker confirmation of AD pathology, and may therefore underestimate true prevalence of APOE ε4 in AD. We assessed APOE ε4 prevalence in amyloid-positive subjects only. Methods: In this cross-sectional, multicenter study, we combined cohorts from 57 centers worldwide. This yielded a total sample of 3,451 amyloid-positive subjects as assessed by cerebrospinal fluid or positron emission tomography, including 853 with a clinical diagnosis of AD dementia, 1,810 with mild cognitive impairment (prodromal AD) and 788 controls (preclinical AD). APOE ε4 prevalence was determined for
P515
Table 1 Demographic characteristics according to diagnosis Diagnosis
N Age Sex (% male) MMSE (mean) Education (mean, y) APOE ε4 (% positive)
Preclinical AD
Prodromal AD
AD dementia
788 72.6 53 28.8 13.9 51
1810 71.8 47 26.5 12.9 64
853 69.1 45 21.6 12.9 66
AD – Alzheimer’s disease, MMSE – Mini mental state examination, APOE – Apolipoprotein E.
all diagnostic groups and generalized estimating equation models were used to assess effects of age, sex and education. Results: APOE ε4 prevalence was 66% in AD dementia, 64% in prodromal AD and 51% in preclinical AD. Prevalence decreased with advancing age in preclinical (b for change in prevalence per year ¼ -0.02, p < 0.05) and prodromal AD (b: -0.03, p < 0.01), but not in AD dementia (p ¼ 0.71). There were no effects of sex or education on APOE ε4 prevalence. Conclusions: We found higher APOE ε4 prevalence in AD dementia subjects compared to previous studies. These earlier studies did not require biomarker confirmation of amyloid pathology, which likely resulted in an underestimation of true APOE ε4 prevalence. APOE ε4 accelerates the age of onset of AD dementia, as the prevalence decreased with age in preclinical and prodromal subjects. The lack of an age effect in the AD dementia group may be partly caused by atypical variants of AD (often APOE ε4 non-carriers), which are overrepresented among early onset AD dementia patients. To our knowledge, this is the first assessment of APOE ε4 carrier prevalence in an amyloid-positive population. Our results emphasize the importance of APOE ε4 for development of AD and suggest that therapies targeting APOE ε4 function may be important for disease prevention.
P1-576
A TEN-YEAR FOLLOW-UP OF ADIPOSITY INDICATORS AND DEMENTIA IN ADULTS AGE 70-YEARS AND OLDER: THE GOTHENBURG BIRTH COHORT STUDIES
Deborah R. Gustafson1,2,3, Ilse Arnoldussen4, Valter Sundh5, 8 € Kristoffer B€ackman6, Silke Kern7, Svante Ostling , Ingmar Skoog7, 4 1 Amanda Kiliaan , University of Sk€ovde, Sk€ovde, Sweden; 2University of Gothenburg, Gothenburg, Sweden; 3SUNY Downstate Medical Center, Brooklyn, NY, USA; 4Radboud University Medical Center, Nijmegen, Netherlands; 5Neuroscience and Physiology, Gothenburg, Sweden; 6 University of Gothenburg, M€olndal, Sweden; 7Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, M€olndal, Sweden; 8Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, M€olndal, Sweden. Contact e-mail: [email protected] Background: The adiposity indicators body mass index (BMI), Figure 1. Association of age with APOE ε4 prevalence according to diagnosis. This graphical representation of APOE ε4 prevalence as a function of age in amyloid-beta positive patients shows a decrease of prevalence with advancing age in preclinical AD and prodromal AD, but not in AD dementia. AD – Alzheimer’s disease, APOE – Apolipoprotein E.
waist-hip ratio (WHR), leptin and adiponectin could be useful markers of dementia as both physical and metabolic changes occur during the preclinical dementia phase. Methods: Dementia occurrence was associated with BMI, WHR, leptin and adiponectin levels in 924 Swedish elderly without dementia participating in the Gothenburg Birth Cohort studies. These adults, age 70 years and older at baseline, were followed over a 10 year period beginning in 2000, with follow-ups in 2005 and 2009. Results: Multivariate