Long description of table:

Table titled “Replications and Derivatives of My Work.”
The table has three columns labeled: Pillar, My Contribution, and Their Publication (Replication Quote).

Row 1

  • Pillar: Japan – Genetic Allostasis

  • My Contribution: “In autistics, gene mutations activate an internal stress response.”

  • Their Publication (Replication Quote):
    “We performed canonical pathway analysis using Ingenuity Pathways Analysis (IPA). Three major translational pathways, EIF2 signaling, regulation of eIF4 and p70S6K signaling, and mTOR signaling, were enriched through all 12 cell lines containing ASD-associated CNVs. These pathways seemed common and convergent regardless of cell type and psychiatric disorders.”

Row 2

  • Pillar: Brazil – BH4 Shunt Pivot

  • My Contribution: “That activates a BH4 shunt. (Autism trait symptoms)”

  • Their Publication (Replication Quote):
    “Under physiologic conditions, GTPCH is the rate-controlling enzyme in the BH4 pathway. GCH1, which is positively regulated by inflammatory and oxidant mediators, is markedly upregulated during inflammation, leading to innate immune system activation for multiple acute and chronic conditions. A robust body of evidence gathered from various clinical trials suggests that dysfunction in the BH4 pathway may impair the activity of peptidergic, monoaminergic, and NO-dependent neurons in individuals with ASD.”

Row 3

  • Pillar: Stanford – CSTL Dysregulation

  • My Contribution: “The BH4 shunt dysregulates neurotransmitters and E/I balance in the CSTL (producing autism-specific traits).”

  • Their Publication (Replication Quote):
    “Burst firing in RT neurons accompanied by elevated T-type calcium currents. In vivo fiber photometry confirmed behavior-associated increases in RT population activity. RT hyperexcitability identified as a potential therapeutic mechanism driver of ASD.”

Row 4

  • Pillar: Brazil – Epigenetic BioToggle / NOS Uncoupling

  • My Contribution: “The same BH4 shunt activates epigenetic redox-sensitive protein shunts via chronic NOS uncoupling. This creates biochemically linked comorbidities.”

  • Their Publication (Replication Quote):
    “NOSII relies on increased biosynthesis of BH4 to produce large quantities of NO. During persistent inflammation, sustained BH4 demand leads to NOSII uncoupling, resulting in superoxide instead of NO. Peroxynitrite depletes BH4 stores and triggers GTPCH proteolysis, creating a deleterious cycle in ASD.”

Row 5

  • Pillar: Princeton – Phenotype Linkage Methods

  • My Contribution: “Different phenotypes result from clustered traits of autism and comorbid conditions, which link to distinct biochemical pathways.”

  • Their Publication (Replication Quote):
    “Phenotypic and clinical outcomes correspond to genetic and molecular programs of common and inherited variation, further characterizing distinct pathways disrupted by the sets of mutations in each class.”