3 results match your criteria: "University Hospital Cologne and Center for Molecular Medicine Cologne (CMMC)[Affiliation]"
Bi-allelic mutations in PRUNE lead to neurodegeneration with spinal motor neuron involvement and hyperCKaemia.
Turk J Pediatr
August 2020
Division of Child Neurology, Department of Pediatrics, Dokuz Eylül University School of Medicine, İzmir.
Okur D, Daimagüler HS, Ersen Danyeli A, Tekgül H, Wang H, Wunderlich G, Çırak S, Yiş U. Bi-allelic mutations in PRUNE lead to neurodegeneration with spinal motor neuron involvement and hyperCKaemia. Turk J Pediatr 2019; 61: 931-936.
View Article and Find Full Text PDFDie another day: a painless path to longevity.
Cell
May 2014
Max-Planck-Institute for Neurological Research, Gleueler Strasse 50a, 50931 Köln, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne and Center for Molecular Medicine Cologne (CMMC), Zülpicher Strasse 47a, 50674 Köln, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Ageing Associated Diseases (CECAD), Zülpicher Str. 47a, 50674 Köln, Germany. Electronic address:
Riera et al. identify a neuroendocrine circuit that controls longevity and the age-dependent onset of metabolic decline via the pain-transducing channel TRPV1. Thus, pharmacological inhibition of TRPV1 may provide a new approach to treat not only metabolic disorders but also a broader range of age-related pathologies.
View Article and Find Full Text PDFPerinatal programming of metabolic diseases: role of insulin in the development of hypothalamic neurocircuits.
Endocrinol Metab Clin North Am
March 2013
Department of Mouse Genetics and Metabolism, University Hospital Cologne and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Köln 50674, Germany.
It is increasingly accepted that the metabolic future of an individual can be programmed as early as at developmental stages. For instance, offspring of diabetic mothers have a greater risk of becoming obese and diabetic later in life. Animal studies have demonstrated that hyperinsulinemia and/or hyperglycemia during perinatal life permanently impair the organization and long-term function of hypothalamic networks that control appetite and glucose homeostasis.
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