Effects of Intranasal Insulin on Controlled Cortical Impact Brain Injury in a Rat Model
Abstract
Traumatic brain injury (TBI) is a serious health problem that affects approximately 2.5 million people in the United States each year and causes serious cognitive and physical deficits lasting long after the acute injury. Physical and cognitive limitations, as well as anxiety, have been identified as common and critical issues after TBI. One of the subcortical structures that is often damaged and is classically linked to memory and anxiety is the hippocampus. TBI results in a marked reduction in glucose uptake in the brain, including in the hippocampus, which can last for years after injury. Currently, there is no effective treatment devised for the deficits that develop after TBI. An additional complication is gaining access of the treatment to the central nervous system (CNS) because of the protection from the blood-brain barrier (BBB). Research has demonstrated that some drugs, such as insulin, can reach the CNS by intranasal administration through the olfactory and trigeminal pathways. Intranasal insulin administration has been shown to increase cerebral glucose uptake and improve memory function in normal subjects and patients with Alzheimer's disease, without affecting systemic blood glucose or insulin levels.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 27, 2019
- Accession Number
- AD1181538
Entities
People
- John R. Reed
Organizations
- Uniformed Services University of the Health Sciences