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Metropolitan Government of Nashville-Davidson (balance), TN, United States

Weinstein J.J.,Vanderbilt University | Rogers B.P.,Vanderbilt University | Taylor W.D.,Vanderbilt University | Taylor W.D.,The Geriatric Research | And 5 more authors.
Psychiatry Research - Neuroimaging | Year: 2015

Depression remains a great societal burden and a major treatment challenge. Most antidepressant medications target serotonergic raphé nuclei. Acute tryptophan depletion (ATD) modulates serotonin function. To better understand the raphé's role in mood networks, we studied raphé functional connectivity in depression. Fifteen depressed patients were treated with sertraline for 12 weeks and scanned during ATD and sham conditions. Based on our previous findings in a separate cohort, resting state MRI functional connectivity between raphé and other depression-related regions (ROIs) was analyzed in narrow frequency bands. ATD decreased raphé functional connectivity with the bilateral thalamus within 0.025-0.05. Hz, and also decreased raphé functional connectivity with the right pregenual anterior cingulate cortex within 0.05-0.1. Hz. Using the control broadband filter 0.01-0.1. Hz, no significant differences in raphé-ROI functional connectivity were observed. Post-hoc analysis by remission status suggested increased raphé functional connectivity with left pregenual anterior cingulate cortex in remitters (n=10) and decreased raphé functional connectivity with left thalamus in non-remitters (n=5), both within 0.025-0.05. Hz. Reducing serotonin function appears to alter coordination of these mood-related networks in specific, low frequency ranges. For examination of effects of reduced serotonin function on mood-related networks, specific low frequency BOLD fMRI signals can identify regions implicated in neural circuitry and may enable clinically-relevant interpretation of functional connectivity measures. The biological significance of these low frequency signals detected in the raphé merits further study. © 2015 Elsevier Ireland Ltd. Source


Salmon A.B.,University of Texas Health Science Center at San Antonio | Salmon A.B.,The Geriatric Research | Lerner C.,Drexel University | Ikeno Y.,University of Texas Health Science Center at San Antonio | And 4 more authors.
American Journal of Physiology - Endocrinology and Metabolism | Year: 2015

The extension of lifespan due to reduced insulin-like growth factor 1 (IGF-I) signaling in mice has been proposed to be mediated through alterations in metabolism. Previously, we showed that mice homozygous for an insertion in the Igf1 allele have reduced levels of IGF-I, are smaller, and have an extension of maximum lifespan. Here, we tested whether this specific reduction of IGF-I alters glucose metabolism both on normal rodent chow and in response to high-fat feeding. We found that female IGF-I-deficient mice were lean on a standard rodent diet but paradoxically displayed an insulin-resistant phenotype. However, these mice gained significantly less weight than normal controls when placed on a high-fat diet. In control animals, insulin response was significantly impaired by high-fat feeding, whereas IGF-I-deficient mice showed a much smaller shift in insulin response after high-fat feeding. Gluconeogenesis was also elevated in the IGF-I-deficient mice relative to controls on both normal and high-fat diet. An analysis of metabolism and respiratory quotient over 24 h indicated that the IGF-I-deficient mice preferentially utilized fatty acids as an energy source when placed on a high-fat diet. These results indicate that reduction in the circulating and tissue IGF-I levels can produce a metabolic phenotype in female mice that increases peripheral insulin resistance but renders animals resistant to the deleterious effects of high-fat feeding. © 2015 the American Physiological Society. Source


Kochar J.,Beth Israel Deaconess Medical Center | Kochar J.,Harvard University | Gaziano J.M.,Harvard University | Gaziano J.M.,Brigham and Womens Hospital | And 6 more authors.
Aging and Disease | Year: 2011

Coronary heart disease (CHD) is an important cause of morbidity and mortality in the US. A variety of dietary components and patterns have been suggested to decrease the risk of CHD. The current review examines the epidemiological evidence lending support to beneficial effects of dietary factors on CHD risk. The current literature strongly supports the notion that Mediterranean diet, omega-3 (n-3) fatty acids, flavonoids and polyphenols, dietary fiber, and whole grains confer protection against CHD. Overall, there is no evidence that vitamin intake reduces the risk of incident CHD and data on the role of garlic in CHD prevention are equivocal. Source


Taylor W.D.,The Geriatric Research | Taylor W.D.,Vanderbilt University | Boyd B.,Vanderbilt University | Turner R.,Vanderbilt University | And 5 more authors.
Brain Imaging and Behavior | Year: 2016

The APOE ε4 allele is associated with cognitive deficits and brain atrophy in older adults, but studies in younger adults are mixed. We examined APOE genotype effects on cognition and brain structure in younger adults and whether genotype effects differed by age and with presence of depression. 157 adults (32 % ε4 carriers, 46 % depressed) between 20 and 50 years of age completed neuropsychological testing, 131 of which also completed 3 T cranial MRI. We did not observe a direct effect of APOE genotype on cognitive performance or structural MRI measures. A significant genotype by age interaction was observed for executive function, where age had less of an effect on executive function in ε4 carriers. Similar interactions were observed for the entorhinal cortex, rostral and caudal anterior cingulate cortex and parahippocampal gyrus, where the effect of age on regional volumes was reduced in ε4 carriers. There were no significant interactions between APOE genotype and depression diagnosis. The ε4 allele benefits younger adults by allowing them to maintain executive function performance and volumes of cingulate and temporal cortex regions with aging, at least through age fifty years. © 2016 Springer Science+Business Media New York Source

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