Autism Spectrum Rectification Process (ASRP) Steps

A quick scan of the following ASD Processing steps can provide an insight into the complexity of this childrens' disorder. Not every child with ASD requires every step but the troubling nature and potential complexity of this disorder should be readily apparent. In about 20% of ASD cases a lack of appropriate autophagic pruning (e.g. elimination) of neural synapses occurs which results in a certain amount of extra choatic neural data processing. Conversely, in about 60 % of the cases there is reorganization of neural circuits that includes inappropriate or contradictory processing of sensory data such as visual, auditory and olfactory data input cues--such that the affected child interprets sensory data, social cues, body language, etc. as just the opposite of normal or what might normally be expected.

It should be understood that we cannot promise a complete recovery from this disability but rather we should be able to achieve significant improvement over some period of months up to and even possibly exceeding a year. Also, as neural development is intense in infancy, the earlier we can deal with this disorder the better. The NG ASD regimen will also include other relevant NG Processes and the effectiveness of our work and the child's progress can also be complimented by certain exercises such as brain gym © and super brain yoga ©.

1) Pre-Process Steps and Instructions
2) Impediments Utility Step
3) Process Flow Intelligence Installed
4) Call for and Installation of EDOCAM Utility
5) Call for and installation of ESSWFCR Utility
6) Call to Celestial Field Orientation Attunement Utility
7) Comprehensive Process Flow Compression and Auto Scheduling Instructions
8) Infantile Reduced Attention to Audiovisual Integration & Synchrony in ASD
9) Associated Autophagic Abnormalities
10) Synaptic (Neural) Spine Abnormalities
11) Dendritic Spine Density Abnormalities
12) Misshaping/Shaping Dendritic Spines: mTORC1-Dependent Macroautophagy
13) mTOR as a Central Regulator of Cellular Processes
14) Elevated mTORC1, Reduced Autophagy & Increased Spine Density
15) mTORC-1 Signaling and Autophagic Normalization
16) mTORC-1 Dependent Translation-Independent Signaling Cascade Effects
17) mTOR, Social Interaction Deficits, Mutations & Common Biological Pathways
18) Social Cue Processing Support in the Posterior Superior Temporal Sulcus (pSTS) & the Temporo-    Parietal Junction (TPJ)

19) Restoration of Appropriate Autophagic Pruning
20) Postzygotic Mosaic Mutations Relevant to ASD
21) Pertinent Timeline & Location of Mosaic Mutations
22) Exonic Mosaic Mutations Risk Contribution
23) Dysregulated Protein Synthesis
24) Excessive Protein Synthesis, Lysosome Effects & Other Cellular Anomalies
25) Temporal Cortex Involvement
26) Altered Responses to Social Chemosignals
27) Misreading of Emotional Cues & Impaired Social Communication
28) Exaggerated Cap-Dependent Translation with Synaptic & Associated Behavioral Aberrations
29) Relationship of Sense of Smell to Early Development
30) Overexpression in the EIF4E Protein Coding Gene
31) Potential Role of Single Nucleotide Insertion in the EIF4E Promoter
32) Increased EIF4E Expression in the Striatum & Hippocampus
33) The Role of mGluR’s (Metabotropic Glutamate Receptors)
34) Abnormal mGluR5 Signaling & Signaling Complexes
35) mGluR5–Homer (Scaffold Protein) Regulate Signaling to PI3K & mTOR
36) Associated Homer-mGluR5 Scaffold Functions
37) Overactivated mGluR Signaling & Aberrant Protein Synthesis
38) Protein Translation & Induction of Translation-Dependent Long-term Synaptic Plasticity
39) Modulation of PIKE (Pl 3-Kinease Enhancer)
40) Dysregulated mTOR Signaling, Impaired Synaptic Plasticity, Aberrant Spine Morphology
41) mTORC2 and its role in ASD's
42) Role of Dysregulation of mTOR-Dependent Signaling
43) Decreased Interhemispheric Functional Connectivity
44) Autistic Abnormalities in Long-range, Functional Connectivity
45) White Matter Pathways and Corpus Callosal Volume
46) Attenuated Transcallosal Connectivity Further Identified in ASD
47) Latent and Abnormal Functional Connectivity Circuits
48) Related Interhemispheric Communication Degradation & Constraints
49) Low Frequency Fluctuations in Cerebral Blood Flow, Hyper & Hypoconnectivity
50) Abnormal or Disrupted Network Connectivity Regions Identified
51) Frontal Lobe Abnormalities Associated with Severe Higher-Order Impairment
52) Latent Differentially Expressed Networks Identified
53) High Degree of Organization in Related Disrupted Neural Networks
54) Striatal Direct Pathway 2-Arachidonoylglycerol Signaling in Sociability & Repetitive Behavior
55) Potential Role of Excessive Glyphosate Ingestion
56) Neuroimmune Role of Glia in ASD
57) Glial Surveillance & Regulation of Neural Environments
58) Cerebellar Glial Hyperactivity & Purkinje Cells Role in ASD
59) Potential Beneficial Microglia & Astrocyte Modulation
60) The Gut–Brain Axis in Childhood Developmental Disorders
61) Associated Autistic Intestinal Conditions
62) Autistic Symptom Progression Related to Gastrointestinal Environment
63) Associated Markers of Autistic Related Bowel Disease
64) Associated Lesions, Hyperplasia and Enterocolitis
65) Relationship to Hepatic Encephalopathy Addressed
66) Autistic Related Intestinal Pathology Summary and Rectification
67) Session Scan of Known/Unknown Genes that Contribute to Symptomatic Behaviors
68) Prioritization of Relevant Scanned Disregulation & Mutation Data
69) Testing Data Correlated with Normal Transhemispheric/Transcollosal Communication Stages
70) Inter & Transhemispheric Communication Rectification and Modulation
71) Maternal/Ancestral Source Factors Addressed
72) ASD Symptomatic Mutations of Maternal/Generational Origin Considered

73) Complex Associations between Affected Neural Regions

74) Individual Variation in ASD Neural and Functional Networks

75) Pervasive Alterations in ASD Neural Processing

76) Abnormal Developmental Chains, Connections & Cascades

77) Higher-Order Cognition Bottlenecks

78) Hyperlexia: When Lexical-to-Phonological Decoding Outpaces Comprehension

79) Inversion of Memory Function & Weakened Central Coherence

80) Executive Deficit and Inadequate Context

81) Complex Anatomical Correlates & Interactions

82) Transient Postnatal Macrencephaly

83) Adult Macrencephalic Compensation

84) Abnormal Oligodendrocyte Regulation, Myelination & Neuronal Populations

85) Neurobiological & Genetic Bases of ASD

86) Family-Based GABA Receptor & Serotonin Transporter Enhancement

87) Maternal & Paternal Genetic Abnormality Contributions

88) DNA Methylation Abnormalities

89) Aminobutyric Acid & Gene Regulation

90) Potential Acetylcholine Protein Function in ASD

91) Elevated Platelet Serotonin (5-HT)

92) Immunological Signaling in ASD

93) Signaling and Rectification Pathways Associated with ASD

94) Some Epigenetic Change Factors

95) Genetic Biomarkers in ASD

96) Metabolic Biomarkers in ASD

97) Oxidative Stress Biomarkers in ASD

98) Mitochondrial Dysfunction Markers in ASD

99) Immune dysregulation & Cytokine evaluation

100) Autoimmunity and Maternal Antibodies

101) Role of Genetic Copy Number Variation (CNV) in ASD

102) Dysbiosis as a Contributive Factor

103) Amino Acids and Neuropeptide Functions

104) Potential Defects in the Major Histocompatibility Complex (MHC)

105) Interdependence of the MHC, Cerebellar Purkinje & Granule Cells

106) Immunity and Neuronal Plasticity in ASD

107) Contributive Factors in Core Dysfunction Including Neural Signal-to-Noise

108) Reverse Engineering Complex ASD Symptoms into Root Resolutions

109) Parental & Child Loss of Self-Definition & Role Identity

110) Other Root Emotions & Mental States Associated with ASD

111) Secondary Emotions and Mental States Associated with NG ASD Clinical Work

112) Empathic Encroachment Effects in ASD Addressed

113) Inadequate Functioning of Behavioral/Historical Mental/Emotional/Neural Database in ASD

114) ASD Data Processing Alterations: What is the Message & Has it Been Received?

115) Parental & Child Loss of Self-Definition & Role Identity
116) Other Root Emotions & Mental States Associated with ASD
117) Secondary/Tertiary Emotions and Mental States Associated with NG ASD Clinical Work

118) ADS Symptom Disorder Payoffs & DIvine Self-Definition Considered & Addressed
119) Empathic Encroachment Effects in ASD Addressed
120) Additional Generational Effects
121) Conclusions
122) Final Process Objectives
123) Call to ERPP Process if Indicated
124) Final Clearing & Modulation Installed