Insulin-like growth factor-I given subcutaneously reduces clinical deficits, decreases lesion severity and upregulates synthesis of myelin proteins in experimental autoimmune encephalomyelitis
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The therapeutic effect of platelet-rich plasma on the experimental autoimmune encephalomyelitis mice
2019, Journal of NeuroimmunologyIntrathecal insulin-like growth factor 1 but not insulin enhances myelin repair in young and aged rats
2017, Neuroscience LettersCitation Excerpt :A recent study has re-invigorated interest in insulin-like growth factor 1 (IGF-1) as a potential therapy for neuro-inflammation [1]. Whereas IGF-1 was shown to be a potent promotor of developmental myelin formation [33], its potential to enhance remyelination remained controversial [6,27,32]. The functionally and structurally related hormone insulin could yet be another approach to boost remyelination.
Kinematic gait parameters are highly sensitive measures of motor deficits and spinal cord injury in mice subjected to experimental autoimmune encephalomyelitis
2017, Behavioural Brain ResearchCitation Excerpt :Second, these decreases were associated with reduced average hip and knee angles over the entire step cycle, suggestive of an inability to extend these joints. These deficits may contribute to the decrease in stride length and walking speed observed for both EAE rodents and MS patients [36,76–78] Two of the most common gait deficits in these neurodegenerative conditions are: 1) decreased ability to lift the foot from the ground causing foot drop and 2) reduced walking speed corresponding to a pronounced weakness in the distal muscles of the leg (ankle dorsal and plantar flexors) [63,70,71]. Consistent with these findings, we have shown that toe height is progressively reduced with increased EAE severity while walking speed is known to be decreased by EAE [9].
The role of growth factors as a therapeutic approach to demyelinating disease
2016, Experimental NeurologyCitation Excerpt :For example, in agreement with the cuprizone results, in acute rat EAE IGF-I, injected peripherally during the onset of disease, reduces maximum clinical scores as well as lesion severity, and promotes a faster recovery (Liu et al., 1995, 1997). It also reduces the size and number of demyelinating lesions and upregulates myelin related protein mRNAs (Yao et al., 1995, 1996). In a chronic relapsing mouse EAE model, IGF-I treatment also reduces clinical deficits (Li et al., 1998).
Neuroprotection in multiple sclerosis: A therapeutic challenge for the next decade
2010, Pharmacology and TherapeuticsInsulin-like growth factor-I mitigates motor coordination deficits associated with neonatal alcohol exposure in rats
2009, Neurotoxicology and TeratologyCitation Excerpt :Thus, interference with IGF-I signaling may contribute to alcohol-related neuroteratogenicity. The possibility that IGF-I could serve as a potential treatment for fetal alcohol effects is strengthened by evidence that IGF-I can protect against other CNS insults [22,107,110], enhancing both neuronal generation and growth as well as white matter production. In fact, IGF-I has been shown to attenuate the neuropathological effects of developmental alcohol exposure.