Sentence examples for addiction pathways from inspiring English sources

Measurements were carried out in the midbrain, the region most closely involved in reward and addiction pathways, as well as in the cerebral cortex and hippocampus.

Ingenuity Pathway Analysis (IPA) was used to produce a comprehensive analysis of the genes commonly shared in these addiction pathways.

Several anatomical regions of the brain are associated with reward and addiction pathways, including the ventral tegmental area, medial prefrontal cortex, hippocampus, ventral striatum (including the nucleus accumbens), and the amygdala (Luthi and Luscher, 2014).

The tremendous genetic variability among inbred mouse strains and our ability to model aspects of addiction with various behavioral paradigms, such as CPP, will eventually lead to the identification of genes and gene networks that influence addiction pathways in the brain and promise to have a profound effect on the treatment of addiction in the clinic.

Correlated structure and activity information on ion channels obtained using this integrated system will open the door for the study of basic physiological and biological systems as well as for defining the underlying mechanisms of pathophysiology and diseases, including neurodegenerative diseases, drug addiction, biological pathways, and protein structures.

Because we are interested in identifying addiction associated pathway members that are polymorphic in humans, but not necessarily polymorphic in mice, our approach identified both candidate genes for mouse phenotypic variation, and biomolecular correlates of the mouse phenotypes.

Approaches to accurately and reproducibly measure multiple nodes in a pathway should allow identification of a tumor's oncogenic pathway addiction as well as highlight potential activated resistance pathways that may result in poor, or limited, response to therapy.

Such activation might be triggered by environmental ligands and be associated with non-oncogene addiction to these pathways.

An intriguing concept that marks a promising future in cancer therapy is the linkage between oncogene addiction and metabolic pathways.

Collectively, these data indicate that E2 promotes pentose phosphate pathway addiction in cells lacking TSC2.

The activation of MEK and then ERK in response to oncogenic NRAS and BRAF mutations is proposed to be the basis of a MAPK pathway addiction by these cells [ 37].