Coordinated Actions of Neurogenesis and Gliogenesis in Nerve Injury Repair and Neuroregeneration

• Published in: International journal of translational medicine Vol. 4; no. 4; pp. 810 - 830
• Main Authors: Chen, Mei-Yu, Chi, Cheng-Yu, Zheng, Chiau-Wei, Wang, Chen-Hung, Chiu, Ing-Ming
• Format: Journal Article
• Language: English
• Published: Jackson MDPI AG 01.12.2024
• Subjects: Alzheimer's disease; Amyotrophic lateral sclerosis; Brain research; Dementia; Disease; FGF1; Growth factors; IL12p80; Kinases; Medical prognosis; Monoclonal antibodies; myelin; nerve injury; Nervous system; neural stem cells; Neurodegeneration; neurodegenerative diseases; Neurogenesis; Proteins; Quality of life; Spinal cord injuries; Stem cells
• ISSN: 2673-8937; 2673-8937
• DOI: 10.3390/ijtm4040053

The failure of endogenous repair mechanisms is a key characteristic of neurological diseases, leading to the inability to restore damaged nerves and resulting in functional impairments. Since the endogenously regenerative capacity of damaged nerves is limited, the enhancement of regenerative potential of quiescent neural stem cells (NSCs) presents as a therapeutic option for neural diseases. Our previous studies have shown exciting progress in treating sciatic nerve injury in mice and rats using NSCs in conjunction with neurotrophic factors such as fibroblast growth factor 1 (FGF1). Additionally, a recently discovered neurotrophic factor, IL12p80, has shown significant therapeutic effects in sciatic nerve injury repair via myelinating oligodendrocytes. IL12p80 induces oligodendrocyte differentiation from NSCs through phosphorylation of Stat3. Therefore, it might be possible to alleviate the myelination defects of oligodendrocytes in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and even schizophrenia through the administration of IL12p80. These applications could shed light on IL12p80 and FGF1, not only in damaged nerve repair, but also in rectifying the oligodendrocytes’ defects in neurodegenerative diseases, such as ALS and MS. Finally, the synergistic effects of neurogenesis-induced FGF1 and myelination-induced IL12 might be able to supplant the need of NSCs for nerve repair and neuroregeneration.