DNA microarray analysis in hippocampus of Wild-type (WT), AtrxΔE2, and 5-aminolevulinic acid (5-ALA) treated AtrxΔE2 mice.

5-ALA that can be metabolized to porphyrins, protoporphyrin IX and hemin antagonizes decreased synaptic plasticity and cognitive deficits seen in ATR-X model (AtrxΔE2) mice. Our findings suggest a potential therapeutic strategy to target G-quadruplexes and decrease cognitive impairment associated with ATR-X syndrome. We administered 5-ALA (3mg/kg, p.o.) to AtrxΔE2 mice daily between post-natal day 30 to 90.