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Manfred M. Fichter

Researcher at Ludwig Maximilian University of Munich

Publications -  269
Citations -  16000

Manfred M. Fichter is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Eating disorders & Anorexia nervosa (differential diagnoses). The author has an hindex of 65, co-authored 266 publications receiving 14167 citations. Previous affiliations of Manfred M. Fichter include Max Planck Society & University of Mainz.

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Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Phil Lee, +606 more
- 12 Dec 2019 - 
TL;DR: Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes.
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Weight gain decreases elevated plasma ghrelin concentrations of patients with anorexia nervosa

TL;DR: Fasting plasma levels of the novel appetite-modulating hormone ghrelin are elevated in anorexia nervosa and return to normal levels after partial weight recovery, suggesting the possible existence of ghrel in resistance in cachectic states such as caused by eating disorders.
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Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa

Hunna J. Watson, +258 more
- 01 Aug 2019 - 
TL;DR: The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index.
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Several Mutations in the Melanocortin-4 Receptor Gene Including a Nonsense and a Frameshift Mutation Associated with Dominantly Inherited Obesity in Humans

TL;DR: The data indicate that mutations in the MC4-R are not uncommon, and support the evidence for dominantly inherited obesity as revealed by the three obese probands with haplo-insufficiency, the functional significance of the missense mutations remains to be determined.