The Whole Spectrum of Alcohol-Related Changes in the CNS: Practical MR and CT Imaging Guidelines for Daily Clinical Use

Keil, Vera C.; Greschus, Susanne; Schneider, Christoph; Hadizadeh, Dariusch R.; Schild, Hans H.

doi:10.1055/s-0035-1553509

Cited by 6 publications

(3 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Together, these changes may reduce function of critical neurocircuitry in the brain, and therefore, impede learning and memory, impair executive function and decision-making and reduced connectivity between key brain regions, and thereby contribute to the “relapsing” characteristic of AUD. Clinical evidence for glial damage include MRI scans showing a significant atrophy/decreases in white matter in individuals who have a history of chronic alcohol abuse [ 16 ]. This atrophy is exacerbated in individuals with alcohol-associated deficiency of thiamine, a natural dietary antioxidant [ 16 ].…”

Section: Alcohol Use Disorder: Focus On Pathology Associated With mentioning

confidence: 99%

“…Clinical evidence for glial damage include MRI scans showing a significant atrophy/decreases in white matter in individuals who have a history of chronic alcohol abuse [ 16 ]. This atrophy is exacerbated in individuals with alcohol-associated deficiency of thiamine, a natural dietary antioxidant [ 16 ]. Converging evidence from clinical and preclinical research overwhelmingly support oxidative stress as a key factor implicated in alcohol-mediated damage that affects neurons, oligodendroglia, microglia, astroglia as well as cerebral vasculature [ 13 , 17 , 18 , 19 , 20 ].…”

Section: Alcohol Use Disorder: Focus On Pathology Associated With mentioning

confidence: 99%

See 1 more Smart Citation

Platelet Endothelial Cell Adhesion Molecule-1 and Oligodendrogenesis: Significance in Alcohol Use Disorders

et al. 2017

View full text Add to dashboard Cite

Alcoholism is a chronic relapsing disorder with few therapeutic strategies that address the core pathophysiology. Brain tissue loss and oxidative damage are key components of alcoholism, such that reversal of these phenomena may help break the addictive cycle in alcohol use disorder (AUD). The current review focuses on platelet endothelial cell adhesion molecule 1 (PECAM-1), a key modulator of the cerebral endothelial integrity and neuroinflammation, and a targetable transmembrane protein whose interaction within AUD has not been well explored. The current review will elaborate on the function of PECAM-1 in physiology and pathology and infer its contribution in AUD neuropathology. Recent research reveals that oligodendrocytes, whose primary function is myelination of neurons in the brain, are a key component in new learning and adaptation to environmental challenges. The current review briefly introduces the role of oligodendrocytes in healthy physiology and neuropathology. Importantly, we will highlight the recent evidence of dysregulation of oligodendrocytes in the context of AUD and then discuss their potential interaction with PECAM-1 on the cerebral endothelium.

show abstract

Section: Alcohol Use Disorder: Focus On Pathology Associated With mentioning

confidence: 99%

Section: Alcohol Use Disorder: Focus On Pathology Associated With mentioning

confidence: 99%

Platelet Endothelial Cell Adhesion Molecule-1 and Oligodendrogenesis: Significance in Alcohol Use Disorders

et al. 2017

View full text Add to dashboard Cite

show abstract

“…After the liver, the brain is the organ most frequently involved in systemic alcohol toxicity causing a wide spectrum of structural and functional changes in addition to alcohol addiction [52]. This produces an important health-related systemic impact [53].…”

Section: Strategies To Decrease Factors Inducing Heart Damagementioning

confidence: 99%

New Treatment Strategies for Alcohol-Induced Heart Damage

Fernández‐Solà

Porta

2016

IJMS

View full text Add to dashboard Cite

High-dose alcohol misuse induces multiple noxious cardiac effects, including myocyte hypertrophy and necrosis, interstitial fibrosis, decreased ventricular contraction and ventricle enlargement. These effects produce diastolic and systolic ventricular dysfunction leading to congestive heart failure, arrhythmias and an increased death rate. There are multiple, dose-dependent, synchronic and synergistic mechanisms of alcohol-induced cardiac damage. Ethanol alters membrane permeability and composition, interferes with receptors and intracellular transients, induces oxidative, metabolic and energy damage, decreases protein synthesis, excitation-contraction coupling and increases cell apoptosis. In addition, ethanol decreases myocyte protective and repair mechanisms and their regeneration. Although there are diverse different strategies to directly target alcohol-induced heart damage, they are partially effective, and can only be used as support medication in a multidisciplinary approach. Alcohol abstinence is the preferred goal, but control drinking is useful in alcohol-addicted subjects not able to abstain. Correction of nutrition, ionic and vitamin deficiencies and control of alcohol-related systemic organ damage are compulsory. Recently, several growth factors (myostatin, IGF-1, leptin, ghrelin, miRNA, and ROCK inhibitors) and new cardiomyokines such as FGF21 have been described to regulate cardiac plasticity and decrease cardiac damage, improving cardiac repair mechanisms, and they are promising agents in this field. New potential therapeutic targets aim to control oxidative damage, myocyte hypertrophy, interstitial fibrosis and persistent apoptosis In addition, stem-cell therapy may improve myocyte regeneration. However, these strategies are not yet approved for clinical use.

show abstract