Page 268 - Flipping book The Adam Paradox Hypothesis - Second Edition.pdf

The Ādam Paradox Hypothesis 245
Neuroscience
What to Do
1. Refine simulations with neural network AI, validating against human
behavioral experiments.
Early Phase I models are refined with advanced AI neural networks that
can handle recursion, memory, and symbolic processing more realistically.
These simulations are cross-checked against behavioral experiments (e.g.,
language tasks, rule-learning) in humans today.
2. Link organoid results with MRI studies on modern human populations
carrying FOXP2 or HAR1 variants.
Phase I organoid findings (lab-grown brain tissue) are compared to real
human brain imaging.
Example: If organoids with a FOXP2 mutation show disrupted oscillations,
do humans with rare FOXP2 mutations show parallel disruptions on
MRI/EEG?
Tools
Advanced neural network AI that can simulate recursion, memory, and
symbolic reasoning at higher complexity.
Organoid + CRISPR editing pipelines — systematically editing FOXP2,
HAR1, and other regulatory variants, then comparing results across labs.
Multi-modal neuroimaging (combined fMRI, EEG, MEG, DTI) in real
human populations with FOXP2/HAR1 variation, integrated with
organoid results.
Cross-validation platforms — linking computational predictions ↔ lab
organoids ↔ living human brain scans.
Expected Outcome
Stronger evidence connecting specific regulatory variants to observable
cognitive and neural outcomes.
A unified model bridging DNA → brain activity → symbolic behavior.
Likely Scenario
By Phase II, expect converging evidence that small regulatory tweaks
measurably impact symbolic cognition.
This will likely validate APH’s claim that a regulatory ignition network
could have triggered the leap around ~70kya.