Structural and functional changes in the central nervous system in the course of anorexia nervosa

Abstract

New achievements within structural and functional imaging of central nervous system offer a basis for better understanding of the mechanisms underlying many mental disorders. In everyday clinical practice, we encounter many difficulties in the therapy of eating disorders. They are caused by a complex psychopathological picture, varied grounds of the problems experienced by patients, often poor motivation for active participation in the treatment process, difficulties in communication between patients and therapeutic staff, and various biological conditions of eating disorders. In this paper, the latest reports on new concepts and methods of diagnosis and treatment of anorexia nervosa have been analyzed. The selection of the analyzed publications was based on the criteria taking into account the time of publication, the size of research cohorts, as well as the experience of research teams in the field of nutritional disorders, confirmed by the number of works and their citations. The work aims to spread current information on anorexia nervosa neurobiology that would allow for determining the brain regions involved in the regulation of food intake, and consequently that may be a potential place where neurobiochemical processes responsible for eating disorders occur. In addition, using modern methods of structural imaging, the authors want to show some of the morphometric variations, particularly within white matter, occurring in patients suffering from anorexia nervosa, as well as those evaluated with magnetoencephalography of processes associated with the neuronal processing of information related to food intake. For example as regards anorexia nervosa, it was possible to localize the areas associated with eating disorders and broaden our knowledge about the changes in these areas that cause and accompany the illness. The described in this paper research studies using diffusion MRI fiber tractography showed the presence of changes in the white matter pathways of the brain, especially in the corpus callosum, which indicate a reduced content of myelin. These changes probably reflect malnutrition, and directly represent the effect of lipid deficiency. This leads to a weakening of the structure, and even cell death. In addition, there are more and more reports that show the normal volume of brain cells in patients with long-term remission of anorexia. It was also shown that in patients in remission stage there are functional changes within the amygdala in response to a task not related symptomatologically with anorexia nervosa. The appearing in the scientific literature data stating that in patients with anorexia nervosa there is a reduced density of GFAP + cells of the hippocampus and increased expression of vimentin and nestin, is also worth noting.

Effects of C5a and Receptor CD88 on Glutamate and N-Methyl-D-Aspartic Acid Receptor Expression in the Mouse Model of Optic Neuromyelitis

“…AQP4 is a class of water channel transmembrane protein expressed on the foot processes of astrocytes, which plays a vital role in maintaining the water balance of brain parenchyma, extracellular osmotic pressure, promoting glial cell migration, and changing neuronal activity [ 18 , 19 ]. GFAP is a skeleton protein of astrocytes in the central nervous system playing a crucial conditioning role in the complement-mediated spinal cord and optic nerve injury [ 20 , 21 ]. First, an immunofluorescence assay was used to detect the expression of AQP4 and GFAP in spinal cord tissue and optic nerve tissue, respectively, and spinal cord injury in an in vitro model was rated (with scores).…”