After many years of heavy drinking, alcohol produces pathological alterations in the brain. In many alcoholics these changes culminate in massive social deterioration and disorders of memory and learning.
Severe cognitive impairments occur in approximately 10% of heavy drinkers. Alcoholic dementia is the second leading course of adult dementia in the Western countries, accounting for 10% of the cases, and still represents an unresolved problem. So far no effective pharmacotherapy for memory problems in alcoholics is available.
Nowadays this problem can be approached by innovative research using molecular and epigenetic analyses, which yield new insight into brain pathophysiology. Molecular dysregulations in endogenous opioids – a neurotransmitter system in the brain that is central to reward function and pain control – are supposed to play a critical role in the development of alcoholism and associated cognitive impairment.
Professor Georgy Bakalkin, involved in a research team focusing on biochemical mechanisms underlying neuropsychiatric disorders, will highlight the latest findings on this clinical challenge and presents a novel mechanism and understanding of cognitive deficit in human alcoholics. Thereby an emerging concept that proposes a new target for pharmacotherapy will be discussed, which might lead to innovative therapeutic interventions to improve or prevent alcohol-induced cognitive impairment in patients with alcohol dependence, and may be generalized to other learning and memory disorders.-European College of Neuropsychopharmacology
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#1 Alcoholism
Dysregulation of the endogenous opioid systems may play a critical role in the development of alcoholism and associated cognitive impairment. They characterize these systems in neurocognitive structures. Similarly to human alcoholics, alcohol treatment increased dynorphin content in the PFC cortex and hippocampus, albeit with different time course. The KOP antagonist norbinaltorphimine administered systemically or locally into CA3 region of hippocampus reversed the development of learning deficit. Thus cycles of alcohol intoxication and withdrawal may activate synthesis of dynorphins, which inhibit the release of neurotransmitters such as acetylcholine and glutamate essential for learning and memory.