Role and Importance of IGF-1 in Traumatic Brain Injuries

Abstract

It is increasingly affirmed that most of the long-term consequences of TBI are due to molecular and cellular changes occurring during the acute phase of the injury and which may, afterwards, persist or progress. Understanding how to prevent secondary damage and improve outcome in trauma patients, has been always a target of scientific interest. Plans of studies focused their attention on the posttraumatic neuroendocrine dysfunction in order to achieve a correlation between hormone blood level and TBI outcomes. The somatotropic axis (GH and IGF-1) seems to be the most affected, with different alterations between the acute and late phases. IGF-1 plays an important role in brain growth and development, and it is related to repair responses to damage for both the central and peripheral nervous system. The IGF-1 blood levels result prone to decrease during both the early and late phases after TBI. Despite this, experimental studies on animals have shown that the CNS responds to the injury upregulating the expression of IGF-1; thus it appears to be related to the secondary mechanisms of response to posttraumatic damage. We review the mechanisms involving IGF-1 in TBI, analyzing how its expression and metabolism may affect prognosis and outcome in head trauma patients.

Caloric restriction stabilizes body weight and accelerates behavioral recovery in aged rats after focal ischemia

“…Subsequent to an acute ischemic event, IGF‐1 crosses the disrupted blood–brain barrier and can induce differentiation of neural cells, including neurons, astrocytes, oligodendrocytes, and endothelial cells, in in vitro and animal models of traumatic brain injury and thus may exert its neuroprotective effects (Mangiola et al ., ). In parallel, insulin‐like growth factor binding protein‐3 (IGFBP‐3) modulates the bioavailability, transportation, and localization of insulin‐like growth factor‐I (IGF‐I), in animal stroke models especially when administered intranasally (Liu et al ., ).…”

Reducing the time interval between concussion and voluntary exercise restores motor impairment, short‐term memory, and alterations to gene expression

“…DNA methyltransferase 1 ( Dnmt1 ) is vital for neurological health and plasticity as it regulates tissue specific methylation patterns (Golshani et al ., ; Feng et al ., ). Furthermore, insulin growth factor‐1 (IGF1) plays a significant role in brain growth, development, and repair (Mangiola et al ., ), while perioxome proliferator‐activated receptor‐gamma coactivator 1‐α ( Pgc1‐α ) has been intimately linked to the regulation of energy metabolism and the stimulation of mitochondrial bioenergetics (Ji et al ., ). Finally, telomerase reverse transcriptase (Tert), maintains TL participating in cellular senescence and repair (Liu et al ., ).…”

Palmitate-induced Endoplasmic Reticulum stress and subsequent C/EBPα Homologous Protein activation attenuates leptin and Insulin-like growth factor 1 expression in the brain

“…The conventional consensus posited that leptin and IGF1 cross the blood-brain-barrier (BBB) and consequently elicit their effects by activating their respective receptors, Ob-Rb (leptin receptor isoform b) and IGF1R that are widely expressed in the brain. However, recent evidence has shown that both leptin [5-11] and IGF1 [10, 12, 13] are expressed endogenously in the brain and exert their effects in an autocrine / paracrine fashion. Leptin expression in the brain is critical as it serves as a neurotrophic cytokine that facilitates memory formation and enhances cognition by augmenting synaptogenesis [14].…”