Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer Disease

al-Dahhak, Roula; Khoury, Rita; Qazi, Erum; Grossberg, George T.

doi:10.1016/j.cger.2018.06.008

Cited by 22 publications

(10 citation statements)

References 114 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Traumatic brain injury increases the risk of developing Alzheimer’s disease (Al-Dahhak et al, 2018 ). Based on experimental studies, this involves disruption of the microvasculature, leading to local ischemia that triggers oxidative stress (Leker and Shohami, 2002 ).…”

Section: Fructose Metabolism and Alzheimer’s Diseasementioning

confidence: 99%

Cerebral Fructose Metabolism as a Potential Mechanism Driving Alzheimer’s Disease

Johnson

Gómez‐Pinilla

Nagel

et al. 2020

Front. Aging Neurosci.

View full text Add to dashboard Cite

Section: Fructose Metabolism and Alzheimer’s Diseasementioning

confidence: 99%

Cerebral Fructose Metabolism as a Potential Mechanism Driving Alzheimer’s Disease

Johnson

Gómez‐Pinilla

Nagel

et al. 2020

Front. Aging Neurosci.

View full text Add to dashboard Cite

“…PD, which is caused by the selective degeneration of dopamine and is characterized by bradykinesia and rigidity, is the second most common neurodegenerative disease (Shi et al, 2017). Studies showed that TBI is one of the strong environmental contributing factors for AD and PD (Hayes et al, 2017;Al-Dahhak et al, 2018;Gardner et al, 2018). One of the possible reasons is that TBI causes diffuse axonal injury and leads to proteinopathies.…”

Section: Mechanisms Underlying Tbi-induced Neurodegenerative Diseasesmentioning

confidence: 99%

Will Sirtuins Be Promising Therapeutic Targets for TBI and Associated Neurodegenerative Diseases?

et al. 2020

View full text Add to dashboard Cite

Traumatic brain injury (TBI), a leading cause of morbidity worldwide, induces mechanical, persistent structural, and metabolic abnormalities in neurons and other brain-resident cells. The key pathological features of TBI include neuroinflammation, oxidative stress, excitotoxicity, and mitochondrial dysfunction. These pathological processes persist for a period of time after TBIs. Sirtuins are evolutionarily conserved nicotinamide-adenine dinucleotide (NAD+)-dependent deacetylases and mono-ADP-ribosyl transferases. The mammalian sirtuin family has seven members, referred to as Sirtuin (SIRT) 1-7. Accumulating evidence suggests that SIRT1 and SIRT3 play a neuroprotective role in TBI. Although the evidence is scant, considering the involvement of SIRT2, 4-7 in other brain injury models, they may also intervene in similar pathophysiology in TBI. Neurodegenerative diseases are generally accepted sequelae of TBI. It was found that TBI and neurodegenerative diseases have many similarities and overlaps in pathological features. Besides, sirtuins play some unique roles in some neurodegenerative diseases. Therefore, we propose that sirtuins might be a promising therapeutic target for both TBI and associated neurodegenerative diseases. In this paper, we review the neuroprotective effects of sirtuins on TBI as well as related neurodegeneration and discuss the therapeutic potential of sirtuin modulators.

show abstract

“…TBI is associated with increased risk for psychiatric disorders, PTSD, and AD pathogenesis (Al-Dahhak and others 2018; Becker and others 2018). Even a single incident of TBI can be associated with risk for AD (Kokiko-Cochran and Godbout 2018).…”

Section: Brain Injury Accelerates Ad Pathogenesis In High-risk Indivimentioning

confidence: 99%

Brain Injury–Mediated Neuroinflammatory Response and Alzheimer’s Disease

et al. 2019

View full text Add to dashboard Cite

Traumatic brain injury (TBI) is a major health problem in the United States, which affects about 1.7 million people each year. Glial cells, T-cells, and mast cells perform specific protective functions in different regions of the brain for the recovery of cognitive and motor functions after central nervous system (CNS) injuries including TBI. Chronic neuroinflammatory responses resulting in neuronal death and the accompanying stress following brain injury predisposes or accelerates the onset and progression of Alzheimer’s disease (AD) in high-risk individuals. About 5.7 million Americans are currently living with AD. Immediately following brain injury, mast cells respond by releasing prestored and preactivated mediators and recruit immune cells to the CNS. Blood-brain barrier (BBB), tight junction and adherens junction proteins, neurovascular and gliovascular microstructural rearrangements, and dysfunction associated with increased trafficking of inflammatory mediators and inflammatory cells from the periphery across the BBB leads to increase in the chronic neuroinflammatory reactions following brain injury. In this review, we advance the hypothesis that neuroinflammatory responses resulting from mast cell activation along with the accompanying risk factors such as age, gender, food habits, emotional status, stress, allergic tendency, chronic inflammatory diseases, and certain drugs can accelerate brain injury-associated neuroinflammation, neurodegeneration, and AD pathogenesis.

show abstract

Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer Disease

Cited by 22 publications

References 114 publications

Cerebral Fructose Metabolism as a Potential Mechanism Driving Alzheimer’s Disease

Cerebral Fructose Metabolism as a Potential Mechanism Driving Alzheimer’s Disease

Will Sirtuins Be Promising Therapeutic Targets for TBI and Associated Neurodegenerative Diseases?

Brain Injury–Mediated Neuroinflammatory Response and Alzheimer’s Disease

Contact Info

Product

Resources

About