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Body image distortion is a core symptom of eating disorders. Functional magnetic resonance imaging (fMRI) studies on body image processing, described different patterns of neural response, mainly involving the inferior and superior parietal lobules, and the dorsolateral prefrontal cortex (DLPFC), with conflicting results.
The neural response to the view of their own body pictures (normal size and distorted) was evaluated in 18 female anorexia nervosa (AN) restricting type patients, and in 19 healthy female subjects (HC) using fMRI. Clinical assessment was performed by means of the structured clinical interview for DSM-IV and self-reported questionnaires.
In response to the body image distortion, patients and controls showed an inverse pattern of activation, with the widest extent of activation in the oversize condition in AN, while in the undersize condition in HC. AN and HC showed a similar pattern of neural response to the view of their own body, with an increased activation in the extrastriate body area, superior and inferior parietal lobule and prefrontal areas, although the extent of activation in HC was more limited as compared with AN patients. Increased activity in AN patients, compared with HC, was observed in the DLPFC in response to the oversized body picture and a significant correlation was found in AN patients between DLPFC activation and eating disorder psychopathology.
Our findings suggest the existence of a continuum from normalcy to pathology in neural response to body image, and confirm the clinical relevance of body image distortion in AN, reinforcing the key role of attentive, executive and self-evaluation networks in AN visual processing of own distorted body image.
Coeliac disease (CD) is a multigenic and multifactorial enteropathy triggered by gluten-composing
proteins. A possible involvement of the intestinal Aminopeptidase N (APN) was investigated by an
association analysis. SSCP analysis detected four variants at position 281, 378, 956 and 2957
(referred to no. g178535, GenBank) that were studied in 193 Italian CD families. The haplotypic
combinations were determined from family segregation and pairwise linkage disequilibria
(D′ = D/Dmax) between the polymorphic sites were calculated. Significant D′ values ranged between 0.78
and 0.31. Association with CD was tested by TDT (Transmission Disequilibrium Test) utilizing as
markers the nucleotide substitutions and their haplotypic combinations. No statistically significant
transmission distortion to the probands or to their clinically silent sibs was observed. Our data
exclude an involvement in CD of the tested markers and of further undetected variation in strong
linkage disequilibrium (D′ ≅ 1) with them. The power of the test was not adequate to detect an
association with an unknown polymorphism which is not in complete linkage disequilibrium with
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