scholarly journals Risk and Resilience: The Role of Brain-derived Neurotrophic Factor in Alcohol Use Disorder

2016 ◽  
Vol 3 (4) ◽  
pp. 398-432 ◽  
Author(s):  
Natalie Ceballos ◽  
◽  
Shobhit Sharma
Keyword(s):  
Alcohol Use ◽  
Neurotrophic Factor ◽  
Alcohol Use Disorder ◽  
Brain Derived Neurotrophic Factor ◽  
Risk And Resilience

scholarly journals Human Plasma BDNF Is Associated With Amygdala-Prefrontal Cortex Functional Connectivity and Problem Drinking Behaviors

2019 ◽  
Vol 23 (1) ◽  
pp. 1-11
Author(s):  
Stephanie M Gorka ◽  
Tara Teppen ◽  
Milena Radoman ◽  
K Luan Phan ◽  
Subhash C Pandey
Keyword(s):  
Prefrontal Cortex ◽  
Individual Differences ◽  
Functional Connectivity ◽  
Alcohol Use ◽  
Medial Prefrontal Cortex ◽  
Neurotrophic Factor ◽  
Alcohol Use Disorder ◽  
Brain Derived Neurotrophic Factor ◽  
Drinking Behaviors ◽  
Threat Of Shock

Abstract Background Preclinical studies suggest that decreased levels of brain-derived neurotrophic factor in the amygdala play a role in anxiety and alcohol use disorder. The association between brain-derived neurotrophic factor levels and amygdala function in humans with alcohol use disorder is still unclear, although neuroimaging studies have also implicated the amygdala in alcohol use disorder and suggest that alcohol use disorder is associated with disrupted functional connectivity between the amygdala and prefrontal cortex during aversive states. Methods The current study investigated whether plasma brain-derived neurotrophic factor levels in individuals with and without alcohol use disorder (n = 57) were associated with individual differences in amygdala reactivity and amygdala-prefrontal cortex functional connectivity during 2 forms of aversive responding captured via functional magnetic resonance imaging: anxiety elicited by unpredictable threat of shock and fear elicited by predictable threat of shock. We also examined whether brain-derived neurotrophic factor and brain function were associated with binge drinking episodes and alcohol use disorder age of onset. Results During anxiety, but not fear, lower levels of plasma brain-derived neurotrophic factor were associated with less connectivity between the left amygdala and the medial prefrontal cortex and the inferior frontal gyrus. In addition, within individuals with alcohol use disorder (only), lower levels of brain-derived neurotrophic factor and amygdala-medial prefrontal cortex functional connectivity during anxiety were associated with more binge episodes within the past 60 days and a lower age of alcohol use disorder onset. There were no associations between brain-derived neurotrophic factor levels and focal amygdala task reactivity. Conclusions Together, the results indicate that plasma brain-derived neurotrophic factor levels are related to amygdala circuit functioning in humans, particularly during anxiety, and these individual differences may relate to drinking behaviors.

Determinants of Blood Brain-Derived Neurotrophic Factor Blood Levels in Patients with Alcohol Use Disorder

2017 ◽  
Vol 41 (7) ◽  
pp. 1280-1287 ◽  
Author(s):  
Philippe Nubukpo ◽  
Nicolas Ramoz ◽  
Murielle Girard ◽  
Dominique Malauzat ◽  
Philip Gorwood
Keyword(s):  
Alcohol Use ◽  
Neurotrophic Factor ◽  
Alcohol Use Disorder ◽  
Brain Derived Neurotrophic Factor ◽  
Blood Levels ◽  
Blood Brain

mTORC and PKCε in Regulation of Alcohol Use Disorder

2020 ◽  
Vol 20 (17) ◽  
pp. 1696-1708 ◽  
Author(s):  
Athirah Hanim ◽  
Isa Naina Mohamed ◽  
Rashidi M. Pakri Mohamed ◽  
Srijit Das ◽  
Norefrina Shafinaz Md Nor ◽  
...  
Keyword(s):  
Alcohol Use ◽  
Alcohol Use Disorder ◽  
Alcohol Intake ◽  
Potential Role ◽  
Synaptic Proteins ◽  
Cellular Mechanisms ◽  
Kinase C ◽  
Protein Kinase C Epsilon ◽  
Seeking Behavior

Alcohol use disorder (AUD) is characterized by compulsive binge alcohol intake, leading to various health and social harms. Protein Kinase C epsilon (PKCε), a specific family of PKC isoenzyme, regulates binge alcohol intake, and potentiates alcohol-related cues. Alcohol via upstream kinases like the mammalian target to rapamycin complex 1 (mTORC1) or 2 (mTORC2), may affect the activities of PKCε or vice versa in AUD. mTORC2 phosphorylates PKCε at hydrophobic and turn motif, and was recently reported to be associated with alcohol-seeking behavior, suggesting the potential role of mTORC2-PKCε interactions in the pathophysiology of AUD. mTORC1 regulates translation of synaptic proteins involved in alcohol-induced plasticity. Hence, in this article, we aimed to review the molecular composition of mTORC1 and mTORC2, drugs targeting PKCε, mTORC1, and mTORC2 in AUD, upstream regulation of mTORC1 and mTORC2 in AUD and downstream cellular mechanisms of mTORCs in the pathogenesis of AUD.

Sleep Problems During the Preschool Years and Beyond as a Marker of Risk and Resilience in Substance Use

2018 ◽  
Author(s):  
Maria M. Wong
Keyword(s):  
Substance Use ◽  
Alcohol Use ◽  
Sleep Problems ◽  
Problem Drinking ◽  
Alcohol Problems ◽  
Risk And Resilience ◽  
Regulatory Processes ◽  
Sleep Physiology ◽  
Before And After

Individuals with alcohol problems have well-described disturbances of sleep, but the development of these disturbances both before and after the onset of problem drinking is poorly understood. This chapter first discusses sleep physiology and its measurement in humans. It then examines the functions of sleep and its role in development. Next, it reviews recent research on the relationship between sleep and alcohol use and related problems. Whereas sleep problems (e.g., difficulties falling or staying asleep) increase the risk of early onset of alcohol use and related problems, sleep rhythmicity promotes resilience to the development of alcohol use disorder and problem substance use. Based on existing research, this chapter proposes a theoretical model of sleep and alcohol use, highlighting the role of self-regulatory processes as mediators of this relationship.

Alcohol Use Disorder

2018 ◽  
Author(s):  
Igor Ponomarev
Keyword(s):  
Alcohol Use ◽  
Alcohol Use Disorder ◽  
Critical Discussion ◽  
Epigenetic Mechanisms ◽  
Future Directions ◽  
Clinically Significant ◽  
Early Life Exposures ◽  
The Brain ◽  
Epigenetic Research

Alcohol use disorder (AUD) is characterized by clinically significant impairments in health and social function. Epigenetic mechanisms of gene regulation may provide an attractive explanation for how early life exposures to alcohol contribute to the development of AUD and exert lifelong effects on the brain. This chapter provides a critical discussion of the role of epigenetic mechanisms in AUD etiology and the potential of epigenetic research to improve diagnosis, evaluate risks for alcohol-induced pathologies, and promote development of novel therapies for the prevention and treatment of AUD. Challenges of the current epigenetic approaches and future directions are also discussed.

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