ABSTRACT
Absrtract Acute disseminated encephalomyelitis (ADEM) is an immune-mediated inflammatory demyelinating disorder of the central nervous system that predominantly affects the pediatric population, and it is characterized by an acute or subacute onset of multifocal neurological symptoms. ADEM is typically a monophasic illness, and the majority of cases are associated with either a preceding infection or vaccination. First-line therapy for the disease is intravenous administration of high-dose methylprednisolone, and the long-term prognosis of ADEM is generally favorable.
Subject(s)
Encephalomyelitis, Acute Disseminated , Central Nervous System , Child , Encephalomyelitis, Acute Disseminated/diagnosis , Encephalomyelitis, Acute Disseminated/drug therapy , Humans , Magnetic Resonance Imaging , Prognosis , VaccinationABSTRACT
BACKGROUND: Accumulation of advanced glycation endproducts (AGEs) is thought to be involved in the pathogenesis of dementia, especially Alzheimer's disease. Tissue AGE accumulation can be estimated using the relative simple noninvasive measurement of skin autofluorescence (SAF), a method based on the fluorescent properties of some AGEs. However, possible involvement of tissue AGE accumulation in mild cognitive impairment (MCI) has not been fully investigated. OBJECTIVE: We investigated whether tissue AGE accumulation estimated by SAF is associated with mild cognitive impairment. METHODS: We analyzed 226 community-dwelling subjects. In addition to several atherosclerosis-related clinical parameters, MCI screening test, assessment of brain atrophy, and SAF were performed on people agedâ>â40 years. MCI was assessed using the Japanese version of the MCI screening method. Atrophy of the brain was assessed by examining the temporal horn area (THA) by brain MRI. RESULTS: SAF was significantly higher in participants with MCI than in those with normal cognitive function (2.56±0.55 versus 2.10±0.41; pâ<â0.001). Logistic regression analyses with adjustment for confounding factors including age and THA showed that high SAFâ>â2.27 was significantly related to the presence of MCI (odds, 6.402; 95% CI, 1.590-25.773, pâ=â0.009). CONCLUSION: We found an association between SAF and MCI, which was independent of brain atrophy, in healthy subjects.
Subject(s)
Cognitive Dysfunction/diagnosis , Glycation End Products, Advanced/metabolism , Optical Imaging/methods , Skin/metabolism , Adult , Aged , Aged, 80 and over , Ankle/physiopathology , Benzocaine , Brain/diagnostic imaging , Chloramphenicol , Cholesterol, LDL/blood , Cognitive Dysfunction/epidemiology , Drug Combinations , Female , Humans , Independent Living , Magnetic Resonance Imaging , Male , Middle Aged , Neural Conduction , Nitrofurazone , Retrospective Studies , Skin/diagnostic imagingABSTRACT
OBJECTIVE: The relationship between plasma levels of adiponectin and cardiovascular events is inconclusive. We evaluated the clinical characteristics of people with high plasma adiponectin and high plasma leptin levels. METHODS: Thousand seven hundred participants recruited from visitors to the Anti-Aging Doc were divided into four groups by combining the bipartiles of plasma adiponectin and leptin levels in men and women separately: AL, high adiponectin and high leptin; Al, high adiponectin and low leptin; al, low adiponectin and low leptin; aL, low adiponectin and high leptin. Body composition, including visceral fat area and thigh muscle cross-sectional area (CSA), brachial-ankle pulse wave velocity (baPWV), periventricular hyperintensity, and urinary albumin excretion, were determined. RESULTS: Twenty percent of the studied population fell within the AL group. This group had a significantly higher visceral fat area than the Al group. Thigh muscle CSA was lowest in the AL group among groups. baPWV, brain white matter lesions, and albuminuria findings in the AL group were significantly higher than those of the Al group. Multiple and logistic regression analyses with confounding parameters further confirmed that plasma adiponectin was not an independent determinant for brain and renal small vessel-related disease. CONCLUSION: These findings suggest that the plasma level of adiponectin alone is not enough for the risk stratification of cardiovascular disease. Leptin resistance associated with skeletal muscle loss in addition to obesity may need to be addressed to identify high risk people with high plasma adiponectin levels.