Insulin resistance and related factors in patients with moderate and severe traumatic brain injury

Korkmaz, Nurdan; Kesikburun, Serdar; Atar, Merve Örücü; Sabuncu, Tevfik

doi:10.1007/s11845-022-03147-y

Cited by 2 publications

(1 citation statement)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notably, TBI also induces brain insulin resistance in animal models [ 187 ] and human patients [ 188 , 189 ], which has been proposed to interfere with the ability of insulin to protect synapses against amyloid beta and tau oligomers [ 187 , 190 ]. Furthermore, brain insulin resistance in mice causes greater neurologic impairment after TBI [ 191 ].…”

Section: Tbi and Admentioning

confidence: 99%

Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury

2023

View full text Add to dashboard Cite

Traumatic brain injury (TBI) survivors frequently suffer from chronically progressive complications, including significantly increased risk of developing aging-related neurodegenerative disease. As advances in neurocritical care increase the number of TBI survivors, the impact and awareness of this problem are growing. The mechanisms by which TBI increases the risk of developing aging-related neurodegenerative disease, however, are not completely understood. As a result, there are no protective treatments for patients. Here, we review the current literature surrounding the epidemiology and potential mechanistic relationships between brain injury and aging-related neurodegenerative disease. In addition to increasing the risk for developing all forms of dementia, the most prominent aging-related neurodegenerative conditions that are accelerated by TBI are amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), Parkinson’s disease (PD), and Alzheimer’s disease (AD), with ALS and FTD being the least well-established. Mechanistic links between TBI and all forms of dementia that are reviewed include oxidative stress, dysregulated proteostasis, and neuroinflammation. Disease-specific mechanistic links with TBI that are reviewed include TAR DNA binding protein 43 and motor cortex lesions in ALS and FTD; alpha-synuclein, dopaminergic cell death, and synergistic toxin exposure in PD; and brain insulin resistance, amyloid beta pathology, and tau pathology in AD. While compelling mechanistic links have been identified, significantly expanded investigation in the field is needed to develop therapies to protect TBI survivors from the increased risk of aging-related neurodegenerative disease.

show abstract