Does Brain Repair Itself After Drug Abuse

NIDA Director Dr. Alan I. Leshner

Remarkable enquiry and technological advances in the past two decades have proved that brain disruption and damage play central roles in the consequences of drug corruption and addiction. Knowing the nature of a problem, of course, opens the fashion for systematic attempts to fix it. Thus, today, finding ways to restore normal encephalon role later on it has been changed by drugs is a master goal of NIDA enquiry. (See "NIDA Pursues Many Approaches to Reversing Methamphetamine's Neurotoxic Furnishings") This goal involves two challenges:

• To reverse the brain changes that underlie addiction, and
• To roll back the loss of cognitive and motor functions that occurs when drugs harm and kill brain cells.

To approach the kickoff challenge, NIDA gives top priority to mapping the sequence of neurobiological changes that takes place during the transition from voluntary to compulsive drug taking. Researchers take already identified some of the changes involved in 2 of the key phenomena associated with habit: drug tolerance and drug peckish. With respect to drug tolerance-the abuser's need for increasing amounts of drug to achieve the desired issue-we now know that drugs significantly increase the availability of dopamine, a neurotransmitter that activates the brain'southward pleasure circuits. When cells are exposed to repeated surges of dopamine due to chronic drug corruption, they may eventually become less responsive to dopamine signals. In recent months, researchers presented prove pointing to a specific change in the dopamine receptor molecule that may exist instrumental in this loss of responsiveness.

Finding ways to restore normal brain role after it has been changed by drugs is a main goal of NIDA inquiry.

Equally for drug craving-the intense hunger that drives addicts to seek drugs despite the potent likelihood of adverse consequences-researchers have shown that information technology is related to widespread alterations in brain activity, but especially to changes in the nucleus accumbens area of the forebrain. An important blazon of craving experienced past addicts, chosen cue-induced craving, occurs in the presence of people, places, or things that they have previously associated with their drug taking. Brain imaging studies take shown that cue-induced craving is accompanied past heightened activity in the forebrain, the anterior cingulate, and the prefrontal cortex-key brain areas for mood and memory. A side by side step in agreement craving will exist to larn what brain processes tie drug abusers' memories and then strongly to the desire to take drugs.

Interventions will be used start to finish ongoing brain harm and repair damaged brain cells, and so to retrain the brain.

Researchers take besides made a solid outset toward meeting the 2d challenge posed by drugs' furnishings on the brain: the restoration of cognitive and motor capabilities lost because of drug abuse. Studies have identified specific brain changes that are likely causes of the persistent losses that are caused by many drugs of abuse. For case, they have shown that:

• Inhalants can produce a variety of deleterious effects-including reduced vision and hearing, impaired movement, and lowered cognitive power, sometimes to the point of dementia-past stripping the protective myelin sheath from encephalon fibers;
• Cocaine causes repeated microscopic strokes in the brain, leading to dead spots in the brain's nervus circuitry;
• Methylenedioxymethamphetamine (MDMA) amercement serotonin-producing neurons, which play a direct role in regulating aggression, mood, sexual activity, slumber, and sensitivity to hurting;
• As reported on page 1, methamphetamine amplifies apoptosis-the normal process past which the brain culls defective cells-to the point where it also eliminates healthy cells.

In extreme cases, drugs tin can cause such severe destruction that users become severely disabled. For case, some methamphetamine abusers have developed a syndrome marked past uncontrollable tremors like to those seen in Parkinson'southward disease. The method of heroin self-administration by inhalation known equally "chasing the dragon" has rendered some young people nearly asleep with large encephalon lesions.

To counteract the drug-related encephalon disruptions that produce habit and cerebral and motor problems, researchers are seeking to mobilize two of import brain capacities. First, under the correct circumstances, the brain tin self-repair some types of damage. Second, the brain is plastic-that is, when cell losses disrupt the neural circuits that the brain has been using for a specific role, it can learn to use other circuits to perform that function. Plasticity is extremely powerful, every bit shown past numerous patients' recoveries from extensive cognitive injuries.

Treatments that convalesce some drug-related brain impairment are already here. In fact, in recent months, researchers have demonstrated that methadone therapy ameliorates a item biochemical abnormality in the brains of opiate abusers. The longer patients stayed in therapy, the more this aspect of their brain biochemistry approached normal. NIDA is currently supporting several like projects that use new brain imaging techniques to evaluate the full bear on of current medication and behavioral treatments on brain neurology and biochemistry. Ultimately, such imaging is likely to become an important tool for assessing patients' treatment needs, their progress in treatment, and the effectiveness of treatment approaches.

Ultimately, researchers envision a two-stage process for helping restore drug abusers' dumb abilities. Interventions will be used outset to stop ongoing encephalon impairment and repair damaged brain cells, then to retrain the encephalon. The rationale for this approach is that repairing the brain showtime will restore lost mental resources and capacities that patients then tin utilize in further treatment. Both behavioral and medication treatments may bear witness to be constructive for both stages of treatment. The first stage may benefit from medications already in use to treat neurological conditions that produce brain abnormalities like to those associated with abuse of some drugs. For case, deprenyl (used in Parkinson's disease) and acetylcysteine (being tested in Lou Gehrig'southward disease) have the potential to aid people with drug-related neurological damage.

The new noesis produced by drug abuse research non only brings present goals closer, information technology too makes possible new and further-reaching goals. Today we are applying our understanding of brain processes to the development of treatments that direct target the brain mechanisms of addiction and to the alleviation or reversal of drug-related brain disruption. What we larn in that attempt will undoubtedly pb to even more powerful insights and strategies for reducing drug abuse and habit and their health and social consequences.

Source: https://archives.drugabuse.gov/news-events/nida-notes/2000/09/treating-brain-in-drug-abuse

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