Early IGF-1 Gene Therapy Prevented Oxidative Stress and Cognitive Deficits Induced by Traumatic Brain Injury

Area of Science:

• Neuroscience
• Genetics
• Pharmacology

Background:

• Traumatic Brain Injury (TBI) is a major cause of death and disability, leading to neuroinflammation and oxidative stress (OS).
• Current anti-inflammatory drugs have limited efficacy due to poor blood-brain barrier penetration.
• Insulin-like growth factor 1 (IGF-1) shows potential for neuroprotection and anti-inflammatory effects.

Purpose of the Study:

• To investigate the efficacy of early IGF-1 gene therapy in mitigating OS markers and cognitive deficits following TBI.
• To assess the impact of IGF-1 gene therapy on protein oxidation and lipid peroxidation in TBI-affected brain regions.

Main Methods:

• Male Wistar rats received IGF-1 gene therapy via adenoviral vectors 15 minutes post-TBI.
• Oxidative stress markers (AOPP and MDA) were measured at 60 minutes, 24 hours, and 7 days post-TBI.
• Working memory was evaluated 7 days after TBI to assess cognitive function.

Main Results:

• TBI significantly increased AOPP and MDA levels in the prefrontal cortex, motor cortex, and hippocampus.
• TBI impaired working memory performance 7 days post-injury.
• IGF-1 gene therapy significantly reduced AOPP and MDA levels and prevented cognitive deficits, restoring working memory.

Conclusions:

• Early IGF-1 gene therapy is a potential therapeutic strategy for TBI.
• This approach effectively targets neuroinflammation and prevents behavioral deficits associated with TBI.