Rui Wang1, Laura Fratiglioni2, Grégoria Kalpouzos3, Martin Lövdén3, Erika J Laukka3, Lena Bronge4, Lars-Olof Wahlund5, Lars Bäckman2, Chengxuan Qiu6. 1. Aging Research Center, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet-Stockholm University, Stockholm, Sweden. Electronic address: rui.wang@ki.se. 2. Aging Research Center, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet-Stockholm University, Stockholm, Sweden; Stockholm Gerontology Research Center, Stockholm, Sweden. 3. Aging Research Center, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet-Stockholm University, Stockholm, Sweden. 4. Division of Medical Imaging and Technology, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden. 5. Division of Clinical Geriatrics, Department of NVS, Karolinska University Hospital at Huddinge, Stockholm, Sweden. 6. Aging Research Center, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet-Stockholm University, Stockholm, Sweden. Electronic address: chengxuan.qiu@ki.se.
Abstract
INTRODUCTION: The underlying pathological mechanisms linking cardiovascular burden to cognitive decline remain unclear. METHODS: We investigated the associations of the Framingham general cardiovascular risk score (FGCRS), apolipoprotein E (APOE) ε4, and brain structure with the Mini-Mental State Examination (MMSE) decline using the 9-year follow-up data from Swedish National Study on Aging and Care in Kungsholmen (n = 2189, age ≥60) and the embedded magnetic resonance imaging (MRI) (n = 448) studies. Volumes of white matter hyperintensities (WMHs), total gray matter, ventricles, and hippocampus were assessed in the MRI sample. RESULTS: A higher FGCRS was associated with faster MMSE decline in young-old people (60-72 years) but not in old-old (≥78 years). Larger volumes of cerebral WMHs and ventricles and smaller volumes of total gray matter and hippocampus were all associated with accelerated MMSE decline (P < .01); these associations were stronger among APOE ε4 carriers than noncarriers. Simultaneously entering multiple brain lesion markers as mediators in the model substantially attenuated the association between FGCRS and MMSE decline. DISCUSSION: The effect of cardiovascular risk burden on cognitive deterioration in old age is largely mediated by mixed brain lesions.
INTRODUCTION: The underlying pathological mechanisms linking cardiovascular burden to cognitive decline remain unclear. METHODS: We investigated the associations of the Framingham general cardiovascular risk score (FGCRS), apolipoprotein E (APOE) ε4, and brain structure with the Mini-Mental State Examination (MMSE) decline using the 9-year follow-up data from Swedish National Study on Aging and Care in Kungsholmen (n = 2189, age ≥60) and the embedded magnetic resonance imaging (MRI) (n = 448) studies. Volumes of white matter hyperintensities (WMHs), total gray matter, ventricles, and hippocampus were assessed in the MRI sample. RESULTS: A higher FGCRS was associated with faster MMSE decline in young-old people (60-72 years) but not in old-old (≥78 years). Larger volumes of cerebral WMHs and ventricles and smaller volumes of total gray matter and hippocampus were all associated with accelerated MMSE decline (P < .01); these associations were stronger among APOE ε4 carriers than noncarriers. Simultaneously entering multiple brain lesion markers as mediators in the model substantially attenuated the association between FGCRS and MMSE decline. DISCUSSION: The effect of cardiovascular risk burden on cognitive deterioration in old age is largely mediated by mixed brain lesions.
Keywords:
Aging; Cerebral small-vessel disease; Cognitive decline; Framingham general cardiovascular risk score; Magnetic resonance imaging; Population study
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