Neuman, J., Roeder, N., Richardson, B., Quattrin, T., Hamilton, J. and Thanos, P.K. (2022) High Fat Diet Increases [3H] Flunitrazepam Binding in the Mouse Brain That Is Dependent on the Expression of the Dopamine D2 Gene. Neurochemical Research, 47, 3003-3011.
https://doi.org/10.1007/s11064-022-03644-7

has been cited by the following article:

• TITLE: Hypothesizing That Pediatric Autoimmune Neuropsychiatric Associated Streptococcal (PANDAS) Causes Rapid Onset of Reward Deficiency Syndrome (RDS) Behaviors and May Require Induction of “Dopamine Homeostasis”

  AUTHORS: Kenneth Blum, Catherine A. Dennen, Eric R. Braverman, Ashim Gupta, David Baron, Bernard William Downs, Debasis Bagchi, Panayotis Thanos, Maureen Pollock, Jag Khalsa, Igor Elman, Abdalla Bowirrat, Rajendra D. Badgaiyan

  KEYWORDS: PANDAS, CANS, Reward Deficiency Syndrome, Group A Beta-Hemolytic Streptococcal (GABHS), Pro-Dopamine Regulation, Dopamine Homeostasis, Molecular Mimicry, Lyme, Borrelia

  JOURNAL NAME: Open Journal of Immunology, Vol.12 No.3, September 30, 2022

  ABSTRACT: Pediatric autoimmune neuropsychiatric disorders associated with group A streptococcal infections (PANDAS) is a concept that is used to characterize a subset of children with neuropsychiatric symptoms, tic disorders, or obsessive-compulsive disorder (OCD), whose symptoms are exacerbated by group A streptococcal (GAS) infection. PANDAS has been known to cause a sudden onset of reward deficiency syndrome (RDS). RDS includes multiple disorders that are characterized by dopaminergic signaling dysfunction in the brain reward cascade (BRC), which may result in addiction, depression, avoidant behaviors, anxiety, tic disorders, and/or OCD. According to research by Blum et al., the dopamine receptor D2 (DRD2) gene polymorphisms are important prevalent genetic determinants of RDS. The literature demonstrates that infections like Borrelia and Lyme, as well as other infections like group A beta-hemolytic streptococcal (GABHS), can cause an autoimmune reaction and associated antibodies target dopaminergic loci in the mesolimbic region of the brain, which interferes with brain function and potentially causes RDS-like symptoms/behaviors. The treatment of PANDAS remains controversial, especially since there have been limited efficacy studies to date. We propose an innovative potential treatment for PANDAS based on previous clinical trials using a pro-dopamine regulator known as KB220 variants. Our ongoing research suggests that achieving “dopamine homeostasis” by precision-guided DNA testing and pro-dopamine modulation could result in improved therapeutic outcomes.