TRANSCRANIAL PHOTOBIOMODULATION PROMOTED CHANGES IN MICROGLIA DENSITY IN THE HIPPOCAMPUS AFTER PERINATAL ASPHYXIA

Perinatal asphyxia (PA) is the oxygen deprivation at birth, which commonly occurs in premature births. Hypoxic-ischemic encephalopathy (HIE) is the primary consequence of this condition, affecting 0.1-0.3% of full-term infants but present in 60% of premature infants. Children who experience PA face high mortality rates (20-50%), and survivors often develop permanent neurological sequelae, including cerebral palsy, cognitive deficits, and sensory impairments. The brain is highly susceptible to oxygen deprivation, leading to complex cellular cascades that result in neuroinflammation, cell death, and glial cell loss in vulnerable regions such as the hippocampus (HPC). Microglia play a crucial role in the inflammatory response by its density and polarization into M1 (pro-inflammatory) and M2 (anti-inflammatory) phenotype. Currently, effective therapies for PA sequelae are lacking. However, emerging research suggests that photobiomodulation therapy (PBMT) holds promise in modulating microglia. PBMT modulates biochemical processes that promote neuroprotection, reduce inflammation, and enhance neuronal recovery. Further investigations into the effects of PBMT on microglia could contribute to the development of more effective therapies for PA and other related neurological conditions.