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Updated: Jun 14, 2025

Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury
Seyedeh Parisa Navabi1, Firuzeh Badreh2, Maryam Khombi Shooshtari1
1Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Abstract:
Traumatic brain injury (TBI) is one of the most causes of death and disability among people, leading to a wide range of neurological deficits. The important process of neurogenesis in the hippocampus, which includes the production, maturation and integration of new neurons, is affected by TBI due to microglia activation and the inflammatory response. During brain development, microglia are involved in forming or removing synapses, regulating the number of neurons, and repairing damage. However, in response to injury, activated microglia release a variety of pro-inflammatory cytokines, chemokines and other neurotoxic mediators that exacerbate post-TBI injury. These microglia-related changes can negatively affect hippocampal neurogenesis and disrupt learning and memory processes. To date, the intracellular signaling pathways that trigger microglia activation following TBI, as well as the effects of microglia on hippocampal neurogenesis, are poorly understood. In this review article, we discuss the effects of microglia-induced neuroinflammation on hippocampal neurogenesis following TBI, as well as the intracellular signaling pathways of microglia activation.

