Jun Matsushima1, Toshiro Kawashima2, Hiromi Nabeta2, Yoshiomi Imamura3, Itaru Watanabe4, Yoshito Mizoguchi2, Naoki Kojima5, Shigeto Yamada6, Akira Monji7. 1. Department of Psychiatry, Faculty of Medicine, Saga University, Saga 849-8501, Japan. Electronic address: jun-matsu.77@nifty.com. 2. Department of Psychiatry, Faculty of Medicine, Saga University, Saga 849-8501, Japan. 3. Department of Psychiatry, Faculty of Medicine, Saga University, Saga 849-8501, Japan; Institute of Comparative Studies of International Cultures and Societies, Kurume University, Fukuoka 839-8502, Japan. 4. Department of Psychiatry, Faculty of Medicine, Saga University, Saga 849-8501, Japan; Ureshino Onsen Hospital, Saga 843-0301, Japan. 5. Kojima Hospital, Imari, Saga 848-0121, Japan. 6. St Lucia׳s Hospital, Kurume, Fukuoka 830-0047, Japan. 7. Department of Psychiatry, Faculty of Medicine, Saga University, Saga 849-8501, Japan. Electronic address: amonji@hf.rim.or.jp.
Abstract
BACKGROUND: The relationship between the pathophysiology of dementia and neuroinflammation is well-known. The number of reports stating that depression is a risk factor for dementia has recently been increasing. These epidemiological findings suggest the possibility that both depression and dementia have common pathophysiological backgrounds of neuroinflammation. METHODS: The sample consists of 64 non-demented community-dwelling older participants aged 65 years or over. Participants were assessed at baseline (2004-2006) and 3 years later (2007-2009). Plasma concentration of markers of inflammation (interleukins (IL)-1β, IL-2, IL-6, soluble interleukin-2 receptor (sIL-2R), soluble interleukin-6 receptor (sIL-6R), high sensitivity C-reactive protein (hsCRP) and tumor necrosis factor (TNF)-α) were measured at baseline. Depression symptoms were assessed with the Beck Depression Inventory (BDI) and cognitive decline was assessed with the Mini-Mental State Examination (MMSE), Frontal Assessment Battery (FAB) and Clock Drawing Test (CDT) at baseline and follow-up. All analyses were adjusted for age, gender and years of education. RESULTS: In the cross-sectional analysis, the present study found soluble IL-2 receptor (sIL-2R) to be associated only with the MMSE score at baseline in men. In the longitudinal analysis, none of our inflammatory biomarkers were associated with either depressive symptoms or cognitive decline. LIMITATIONS: The present study consists of small number of participants and body mass index (BMI) scores were not obtained. CONCLUSIONS: Our findings suggest that sIL-2R is associated with current cognitive function in men. None of our inflammatory markers predicted future depressive state or cognitive decline in our community-dwelling healthy older sample.
BACKGROUND: The relationship between the pathophysiology of dementia and neuroinflammation is well-known. The number of reports stating that depression is a risk factor for dementia has recently been increasing. These epidemiological findings suggest the possibility that both depression and dementia have common pathophysiological backgrounds of neuroinflammation. METHODS: The sample consists of 64 non-demented community-dwelling older participants aged 65 years or over. Participants were assessed at baseline (2004-2006) and 3 years later (2007-2009). Plasma concentration of markers of inflammation (interleukins (IL)-1β, IL-2, IL-6, soluble interleukin-2 receptor (sIL-2R), soluble interleukin-6 receptor (sIL-6R), high sensitivity C-reactive protein (hsCRP) and tumor necrosis factor (TNF)-α) were measured at baseline. Depression symptoms were assessed with the Beck Depression Inventory (BDI) and cognitive decline was assessed with the Mini-Mental State Examination (MMSE), Frontal Assessment Battery (FAB) and Clock Drawing Test (CDT) at baseline and follow-up. All analyses were adjusted for age, gender and years of education. RESULTS: In the cross-sectional analysis, the present study found soluble IL-2 receptor (sIL-2R) to be associated only with the MMSE score at baseline in men. In the longitudinal analysis, none of our inflammatory biomarkers were associated with either depressive symptoms or cognitive decline. LIMITATIONS: The present study consists of small number of participants and body mass index (BMI) scores were not obtained. CONCLUSIONS: Our findings suggest that sIL-2R is associated with current cognitive function in men. None of our inflammatory markers predicted future depressive state or cognitive decline in our community-dwelling healthy older sample.
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