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.