Complement C5ar1 Antagonists for the Treatment of Autism Spectrum Disorders

PI DA Iacobas


Our working hypothesis is that PMX53 treatment recovers the ASD-associated alterations of synaptic neurotransmission caused by the modulatory inflammatory pathways on brain circuitries.



Specific Aim 1:

To determine the transcriptomic alterations of the synaptic neurotransmission in the hypothalamic paraventricular node of an ASD rat model.

Specific Aim 2:

To determine the recovery of the synaptic transmission following treatment with the anti-inflammatory agent PMX53.