Vitamin B1 deficiency is a key factor in the development of alcohol-related dementia
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Update time : 2022-06-22 10:41:29
A common consequence of prolonged heavy drinking is cognitive decline, which can even develop into full-blown dementia. However, we don't yet fully understand how alcohol damages the brain. A research team led by Stephan Listabarth from the Division of Social Psychiatry at the Department of Psychiatry and Psychotherapy at the Medical University of Vienna has now proposed a hypothesis that iron deposition in the brain caused by alcohol-induced vitamin B1 deficiency can be inhibited. thought to be a key factor in cognitive decline. The research has been published in the prestigious journal Alzheimer's & Dementia.
In Austria, about 5% of the population is alcohol dependent from the age of 15. This means that approximately 365,000 people are affected by the dangerous health consequences associated with high alcohol consumption. One consequence is a decline in cognitive function, especially memory and refinement. This is called alcoholic dementia. However, we do not yet fully understand the exact pathological mechanism, that is, how the brain is damaged by alcohol.
Researchers Stephan Listabarth, Daniel König and Benjamin Vyssoki of the Department of Social Psychiatry, Department of Psychiatry and Psychotherapy, Medical University of Vienna and Simon Hametner of the Department of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna have now proposed a plausible hypothesis to explain Alcohol-induced brain damage: Cognitive decline is caused by iron deposits in the brain, but vitamin B1 use protects the brain from these deposits.
We know from various neurodegenerative diseases that iron deposits in the brain are responsible for damage to nerve tissue. The deposits were also detected in specific regions of the brain, including the basal ganglia, in heavy drinkers. The hypothesis put forward by the study authors now also explains why iron deposition is so prevalent in this patient group: heavy alcohol consumption leads to elevated iron levels in the blood, as well as deficiency of vitamin B1 (thiamine), which is essential for maintaining the blood-brain barrier. Also important. If these two things happen at the same time, more iron will be deposited inside the brain, eventually leading to oxidative tissue damage.
This newly described role of vitamin B1 in this process may represent a huge advance in our understanding of the development of alcohol-related neurological damage and, in particular, may provide a new target for preventive and therapeutic approaches. Then in the future, it will be possible to take vitamin B1 substitutes continuously as a preventive measure.
The researchers believe it would also be useful to assess the use of drugs that lower iron levels, as is done in other neurodegenerative diseases. The authors of this work have begun planning a prospective clinical study to verify the aforementioned relationship between alcohol dependence, vitamin B1 deficiency, and brain iron deposition, and to provide a basis for future research in the field of alcohol-related dementia.
