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Harnessing Directed Evolution Techniques to Target GABA Receptors, Transporters, and GABA Transaminase in ASD | Alona's Heritage Archive — B7

Harnessing Directed Evolution Techniques to Target GABA Receptors, Transporters, and GABA Transaminase in ASD

Part VII: Synthesis and Future Directions

TAG: #neurology
Latest edit: 16/12/25

by P. De Ceuster — Posted in Research on Dec 16, 2025

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Synthesis: A New Frontier in Neuropharmacology

The convergence of directed evolution, viral gene delivery, and structural biology offers an unprecedented opportunity to address the core molecular deficits of Autism Spectrum Disorder. By transitioning from the blunt instrument of systemic pharmacology to the surgical precision of molecular engineering, we can target the GABAergic system with a level of specificity previously unimaginable.

We have explored how:
1. **Receptor Evolution** can create variants that compensate for low ligand availability or altered kinetics.
2. **Transporter Engineering** can fine-tune the temporal dynamics of inhibition in the synapse.
3. **Metabolic Modulation** of GABA-T can provide "on-demand" inhibition during states of hyperexcitability.
4. **Viral Vectors** enable the delivery of these evolved tools across the blood-brain barrier to specific neuronal populations.

The road ahead is paved with challenges, but the potential reward—restoring the symphony of neural synchrony for millions of individuals—makes it a journey worth taking.

References

[1] Cellot, G., & Cherubini, E. (2014). GABAergic signaling as therapeutic target for autism spectrum disorders. Frontiers in Pediatrics, 2, 70.
[2] Packer, M. S., & Liu, D. R. (2015). Methods for the directed evolution of proteins. Nature Reviews Genetics, 16(7), 379-394.
[3] Kristensen, A. S., et al. (2011). SLC6 neurotransmitter transporters: structure, function, and regulation. Pharmacological Reviews, 63(3), 585-640.
[4] Yocum, A. K., et al. (2019). Mechanism of inactivation of GABA transaminase by the antiepileptic drug vigabatrin. ACS Chemical Biology, 14(1), 3-8.
[5] Deverman, B. E., et al. (2016). Cre-dependent selection yields AAV variants for widespread gene transfer to the adult brain. Nature Biotechnology, 34(2), 204-209.
[6] Rubenstein, J. L., & Merzenich, M. M. (2003). Model of autism: increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior, 2(5), 255-267.
[7] Braat, S., & Kooy, R. F. (2015). The GABAA receptor as a therapeutic target for neurodevelopmental disorders. Neuron, 86(5), 1103-1116.
[8] Cai, Y., et al. (2019). Targeting astrocyte signaling for the treatment of Autism Spectrum Disorder. Neuroscience Bulletin, 35(2), 1-13.

Excerpt from: Harnessing Directed Evolution Techniques to Target GABA Receptors, Transporters, and GABA Transaminase in ASD by Peter De Ceuster


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