Neuroscience: The Brain in Addiction and Recovery National Institute on Alcohol Abuse and Alcoholism NIAAA

by MindTech

Learning about substance-related brain injury can help you understand whether these conditions are permanent or reversible, and it may also encourage you to start the path to recovery from substance use. In that sense, the findings provide new avenues for research that could help illuminate why alcohol has the health effects it does. But one animal study isn’t enough to alter human health recommendations — which already give the OK to a little bit of booze each day.

Neuropsychological tests enable tracking of cognitive skills over time to uncover the effect of alcohol and cannabis use on cognitive development. Alcohol and cannabis are the most commonly used substances during adolescence and are typically initiated during this sensitive neurodevelopmental period. The aim of this review is to provide a comprehensive overview of the most recent literature focused on understanding how these substances affect the developing brain.

Neurochemical Dysfunction in Alcoholism

Further, a 2010 Reuters study found alcohol to be the most harmful substance overall and nearly three times as harmful as cocaine. In fact, one Australian study called cocaine the “perfect heart attack drug” due to both its short and long-term effects on the heart. This makes predicting how the combination might affect mood or thinking exceptionally difficult. For example, alcohol is considered a brain depressant, and it is possible to kill yourself with alcohol. The only methods capable of online detection of the electrical currents in neuronal activity are electromagnetic methods such electroencephalography (EEG), event-related brain potentials (ERP),4 and magnetoencephalography (MEG).

Differences in the pharmacokinetics of various substances determine the duration of their effects on the body and partly account for the differences in their patterns of use. For example, nicotine has a short half-life, which means smokers need to smoke often to maintain the effect. In contrast, THC, the primary psychoactive compound in marijuana, has a much longer half-life. As a result, marijuana smokers do not typically smoke as frequently as tobacco smokers.40 Typical patterns of use are described below for the major classes of addictive substances. However, people often use these substances in combination.41 Additional research is needed to understand how using more than one substance affects the brain and the development and progression of addiction, as well as how use of one substance affects the use of others.

Treatment for Neurological Effects of Drug and Alcohol Misuse

This is accomplished by using specialized tests designed expressly to measure the functions of interest. Among the tests used by scientists to determine the effects of alcoholism on executive functions controlled by the frontal lobes are those that measure problem-solving abilities, reasoning, and the ability to inhibit responses that are irrelevant or inappropriate (Moselhy et al. 2001; Oscar-Berman 2000). Tests to measure spatial cognition controlled by the right hemisphere include those that measure skills important for recognizing faces, as well as those that rely on skills required for reading maps and negotiating two- and three-dimensional space (visuospatial tasks) (Oscar-Berman and Schendan 2000).

Studies have focused on the serotonin transporter (SERT) using [11C] DASB, revealing mixed results with some [148,149] reporting increased levels of SERT whereas others have found no difference or reduced levels of SERT [150]. Research suggests that both quitting and cutting back on your alcohol consumption can provide benefits for your brain by reducing the amount of shrinkage in certain regions. According to Atkinson, previous studies have shown that high levels of alcohol consumption can interfere with alcohol vs drugs this process. About eight months after they began treatment, the higher-risk drinkers had significantly less volume in 12 out of 13 regions when compared with the controls. Together, medication and behavioral health treatments can facilitate functional brain recovery. Neuroimaging studies have shown that conditioned responses to both aversive and positive stimuli are processed and largely mediated by the amygdala, having connections to early sensory processing areas as well as to autonomic centers.

What Do Alcohol and Drugs Do to Your Brain?

Alcohol is thought to activate microglia partially via TLR4 receptors, indeed TLR4 deficiency protected against alcohol induced glial activation and neurotoxicity in a rodent model of chronic alcohol consumption [89]. Analysis of post-mortem brains of patients with Alcohol Use Disorder showed in increase in microglial markers (Iba1 and GluT5) compared with controls [82]. Binge alcohol administration in adolescent rats established microglial proliferation and morphological changes [90]. However, the activation was described as only partial due to the lack of alteration alcohol had on levels of MHC-II or TNF-α expression. Conversely, microglial activation and neurodegeneration were clearly shown in rats exposed to intermittent alcohol treatment [91]. Indeed two-photon microscopy has been used to demonstrate the rapid response of microglia to even single acute alcohol exposure [92].

• Overall, there is no strong, consistent evidence to indicate that low to heavy alcohol use during adolescence or young adulthood disrupts executive functioning maturation across time.
• Mice given low doses of alcohol also showed less inflammation in their brains than mice not exposed to alcohol at all.
• Cortisol, in turn, increases mesencephalic dopaminergic transmission that underlies the activation of alcohol-induced brain reward circuitry (Bowirrat and Oscar-Berman 2005; Gianoulakis 1998; Piazza et al. 1996), in which the amygdala plays an essential role (Koob 2003).
• While only a couple of thousand people die in the United States from an alcohol overdose, some 88,000 deaths a year are caused by alcohol.
• Hippocampal volume reduction also was reported in heavy chronically-drinking, alcohol-dependent subjects compared with nonalcoholic controls (Beresford et al. 2006), with left hippocampal volume reduction being slightly greater than on the right.

Cumulatively, this evidence suggests that alcohol is clearly an activator of microglia, and as previously described upregulation of microglial activation can result in neurotoxicity. However, the extent of alcohol induced microglial activation may well be dependent on the extent and pattern of alcohol exposure. More than 700 articles were captured by the search; and 43 longitudinal studies met inclusion criteria, including 18 studies focused on alcohol use, 13 on cannabis use, and 12 on alcohol and cannabis co-use. Information on levels and typologies of alcohol and cannabis use (see Figure 1), age, and race/ethnicity details are described where available.

KEY TERMS

The following sections provide a brief overview of several neurologic conditions related to alcohol consumption. The development of novel radiotracers with greater specificity for the dopamine D3 receptor allowed characterization of this subtype which has been shown in preclinical models to regulate alcohol consumption. Notably, no difference in binding in the ventral striatum or caudate or putamen was found, however, there was a significantly higher D3 receptor availability in the hypothalamus that was linked to higher lifetime use of alcohol [130].

• Neuroscience provides sensitive techniques for assessing changes in mental abilities and observing brain structure and function over time.
• Well validated tracers for other targets such as those in the serotonergic system do exist, but their use in alcohol dependent individuals is not well characterized.
• With neuroimaging techniques such as computerized tomography (CT) and magnetic resonance imaging (MRI), which allow brain structures to be viewed inside the skull, researchers can study brain anatomy in living patients.
• Nevertheless, there are studies that have suggested differences are not solely attributable to familial risk [55,56], and more research is needed to better understand these risk factors.
• It can affect the normal development of vital organs and parts in teenagers, including the brain, liver, bones, and hormones.
• Prefrontal neurobehavioral dysfunction has been frequently observed in alcoholics with and without the dense amnesia of Korsakoff’s syndrome (Dirksen et al. 2006; Gansler et al. 2000; Oscar-Berman and Evert 1997; Oscar-Berman et al. 2004).

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