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Cardiovascular risk and hippocampal thickness in Alzheimer's disease.

Donix M, Scharf M, Marschner K, Werner A, Sauer C, Gerner A, Nees JA, Meyer S, Donix KL, Von Kummer R, Holthoff VA - Int J Alzheimers Dis (2013)

Bottom Line: Among cognitively healthy people, changes in brain structure and function associated with high blood pressure, diabetes, or other vascular risks suggest differential regional susceptibility to neuronal damage.APOE genotype, a family history of Alzheimer's disease, and age did not influence cortical thickness.This highlights the importance of cardiovascular disease prevention and treatment in patients with Alzheimer's disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry and Psychotherapy, Division of Old Age Psychiatry and Cognitive Neuropsychiatry, University Hospital Carl Gustav Carus, Technische Universität Dresden, 01307 Dresden, Germany ; German Center for Neurodegenerative Diseases (DZNE), 01307 Dresden, Germany.

ABSTRACT
Cardiovascular risk factors influence onset and progression of Alzheimer's disease. Among cognitively healthy people, changes in brain structure and function associated with high blood pressure, diabetes, or other vascular risks suggest differential regional susceptibility to neuronal damage. In patients with Alzheimer's disease, hippocampal and medial temporal lobe atrophy indicate early neuronal loss preferentially in key areas for learning and memory. We wanted to investigate whether this regional cortical thinning would be modulated by cardiovascular risk factors. We utilized high-resolution magnetic resonance imaging and a cortical unfolding technique to determine the cortical thickness of medial temporal subregions in 30 patients with Alzheimer's disease. Cardiovascular risk was assessed using a sex-specific multivariable risk score. Greater cardiovascular risk was associated with cortical thinning in the hippocampus CA2/3/dentate gyrus area but not other hippocampal and medial temporal subregions. APOE genotype, a family history of Alzheimer's disease, and age did not influence cortical thickness. Alzheimer's disease-related atrophy could mask the influence of genetic risk factors or age on regional cortical thickness in medial temporal lobe regions, whereas the impact of vascular risk factors remains detectable. This highlights the importance of cardiovascular disease prevention and treatment in patients with Alzheimer's disease.

No MeSH data available.


Related in: MedlinePlus

CA23DG thickness and cardiovascular risk. This figure shows that greater cardiovascular risk is associated with hippocampal thinning in the CA23DG region (ß = −0.5, P = 0.004) among Alzheimer's disease patients. This effect was not detectable in other medial temporal subregions investigated. We utilized a cardiovascular risk score, developed in the Framingham Heart Study [23], composed of the factors age, total and high-density lipoprotein cholesterol, systolic blood pressure, treatment for hypertension, smoking, and diabetes status.
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fig2: CA23DG thickness and cardiovascular risk. This figure shows that greater cardiovascular risk is associated with hippocampal thinning in the CA23DG region (ß = −0.5, P = 0.004) among Alzheimer's disease patients. This effect was not detectable in other medial temporal subregions investigated. We utilized a cardiovascular risk score, developed in the Framingham Heart Study [23], composed of the factors age, total and high-density lipoprotein cholesterol, systolic blood pressure, treatment for hypertension, smoking, and diabetes status.

Mentions: For patient demographic and cognitive characterization, see Table 1. Utilizing a sex-specific multivariable risk score [23], our patients scored on average 15.3 points (SD 3.1, range 7–22). A high global risk (10-year risk >20%) of coronary, cerebrovascular, and peripheral arterial disease and heart failure [23] would be reflected in a score >17 points for women and >14 points for men. There were 15 patients with this high-risk profile among study participants. In our primary hippocampal region of interest (CA23DG), average cortical thickness across all patients was 2.78 millimeter (SD 0.14, range 2.52–3.04) in CA23DG. The multivariate general linear model revealed significant main effects for cardiovascular risk (F = 4.41, df = 7,14, P = 0.009) and MMSE score (F = 9.15, df = 7,14, P < 0.001) but not for APOE genotype, family history of Alzheimer's disease, and age. Linear regression showed that greater cardiovascular risk was associated with cortical thinning in the CA23DG region (ß = −0.5, P = 0.004, Figure 2) but not in CA1 or other medial temporal lobe subregions. Lower MMSE performance was associated with reduced cortical thickness in several subregions: ERC: ß = 0.4, P = 0.037, PRC: ß = 0.74, P < 0.001, PHC: ß = 0.6, P < 0.001, FUS: ß = 0.58, P < 0.001, and across all regions combined: ß = 0.59, P < 0.001. We did not detect hemispheric differences in the observed effects.


Cardiovascular risk and hippocampal thickness in Alzheimer's disease.

Donix M, Scharf M, Marschner K, Werner A, Sauer C, Gerner A, Nees JA, Meyer S, Donix KL, Von Kummer R, Holthoff VA - Int J Alzheimers Dis (2013)

CA23DG thickness and cardiovascular risk. This figure shows that greater cardiovascular risk is associated with hippocampal thinning in the CA23DG region (ß = −0.5, P = 0.004) among Alzheimer's disease patients. This effect was not detectable in other medial temporal subregions investigated. We utilized a cardiovascular risk score, developed in the Framingham Heart Study [23], composed of the factors age, total and high-density lipoprotein cholesterol, systolic blood pressure, treatment for hypertension, smoking, and diabetes status.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3818844&req=5

fig2: CA23DG thickness and cardiovascular risk. This figure shows that greater cardiovascular risk is associated with hippocampal thinning in the CA23DG region (ß = −0.5, P = 0.004) among Alzheimer's disease patients. This effect was not detectable in other medial temporal subregions investigated. We utilized a cardiovascular risk score, developed in the Framingham Heart Study [23], composed of the factors age, total and high-density lipoprotein cholesterol, systolic blood pressure, treatment for hypertension, smoking, and diabetes status.
Mentions: For patient demographic and cognitive characterization, see Table 1. Utilizing a sex-specific multivariable risk score [23], our patients scored on average 15.3 points (SD 3.1, range 7–22). A high global risk (10-year risk >20%) of coronary, cerebrovascular, and peripheral arterial disease and heart failure [23] would be reflected in a score >17 points for women and >14 points for men. There were 15 patients with this high-risk profile among study participants. In our primary hippocampal region of interest (CA23DG), average cortical thickness across all patients was 2.78 millimeter (SD 0.14, range 2.52–3.04) in CA23DG. The multivariate general linear model revealed significant main effects for cardiovascular risk (F = 4.41, df = 7,14, P = 0.009) and MMSE score (F = 9.15, df = 7,14, P < 0.001) but not for APOE genotype, family history of Alzheimer's disease, and age. Linear regression showed that greater cardiovascular risk was associated with cortical thinning in the CA23DG region (ß = −0.5, P = 0.004, Figure 2) but not in CA1 or other medial temporal lobe subregions. Lower MMSE performance was associated with reduced cortical thickness in several subregions: ERC: ß = 0.4, P = 0.037, PRC: ß = 0.74, P < 0.001, PHC: ß = 0.6, P < 0.001, FUS: ß = 0.58, P < 0.001, and across all regions combined: ß = 0.59, P < 0.001. We did not detect hemispheric differences in the observed effects.

Bottom Line: Among cognitively healthy people, changes in brain structure and function associated with high blood pressure, diabetes, or other vascular risks suggest differential regional susceptibility to neuronal damage.APOE genotype, a family history of Alzheimer's disease, and age did not influence cortical thickness.This highlights the importance of cardiovascular disease prevention and treatment in patients with Alzheimer's disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry and Psychotherapy, Division of Old Age Psychiatry and Cognitive Neuropsychiatry, University Hospital Carl Gustav Carus, Technische Universität Dresden, 01307 Dresden, Germany ; German Center for Neurodegenerative Diseases (DZNE), 01307 Dresden, Germany.

ABSTRACT
Cardiovascular risk factors influence onset and progression of Alzheimer's disease. Among cognitively healthy people, changes in brain structure and function associated with high blood pressure, diabetes, or other vascular risks suggest differential regional susceptibility to neuronal damage. In patients with Alzheimer's disease, hippocampal and medial temporal lobe atrophy indicate early neuronal loss preferentially in key areas for learning and memory. We wanted to investigate whether this regional cortical thinning would be modulated by cardiovascular risk factors. We utilized high-resolution magnetic resonance imaging and a cortical unfolding technique to determine the cortical thickness of medial temporal subregions in 30 patients with Alzheimer's disease. Cardiovascular risk was assessed using a sex-specific multivariable risk score. Greater cardiovascular risk was associated with cortical thinning in the hippocampus CA2/3/dentate gyrus area but not other hippocampal and medial temporal subregions. APOE genotype, a family history of Alzheimer's disease, and age did not influence cortical thickness. Alzheimer's disease-related atrophy could mask the influence of genetic risk factors or age on regional cortical thickness in medial temporal lobe regions, whereas the impact of vascular risk factors remains detectable. This highlights the importance of cardiovascular disease prevention and treatment in patients with Alzheimer's disease.

No MeSH data available.


Related in: MedlinePlus