This vitamin deficiency may lead to alcohol-related dementia

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A common consequence of chronically high alcohol consumption is a decline in cognitive function, which can even progress to full-blown dementia.

However, scientists do not yet fully understand how alcohol damages the brain.

In a new study, researchers have developed a hypothesis whereby iron deposits in the brain—resulting from alcohol-induced vitamin B1 deficiency—can be regarded as key factors in cognitive decline.

The research was conducted by a team at MedUni Vienna.

In Austria, around 5% of the population are alcohol dependent from the age of 15 onwards.

This means that approximately 365,000 people are affected by the dangerous health consequences linked to high alcohol consumption.

One of these consequences is a decline in cognitive function, especially memory and abstraction. This is then referred to as alcohol-related dementia.

However, researchers do not yet fully understand the exact pathomechanism by which the brain is damaged by alcohol.

The team advanced a plausible hypothesis to explain alcohol-induced brain damage: Cognitive deterioration is caused by iron deposits in the brain, but the administration of vitamin B1 could protect the brain from these deposits.

Previous research had shown that iron deposits in the brain are responsible for nerve tissue damage. These deposits can also be detected in specific regions of the brain (including the basal ganglia) in people who drink a lot of alcohol.

The hypothesis advanced by the study authors now also offers an explanation as to why iron deposits are so prevalent in this patient group:

High alcohol consumption results in elevated iron levels in the blood and vitamin B1 (thiamine) deficiency, which, among other things, is important for maintaining the blood-brain barrier.

If these two situations coincide, more iron will be deposited inside the brain, ultimately leading to oxidative tissue damage.

This newly described role of vitamin B1 in this process could represent a huge step forward in our understanding of the development of alcohol-related neurological damage and, in particular, could offer a new point of attack for preventive and therapeutic approaches.

It would then be conceivable to give continuous vitamin B1 substitution in the future as a preventive measure.

The researchers believe it would also be useful to evaluate the use of drugs to reduce iron levels (e.g. chelators), as is already done in other neurodegenerative diseases.

The team has already started planning a prospective clinical study to validate the above-mentioned relationship between alcohol dependency, vitamin B1 deficiency, and cerebral iron deposits and to provide a basis for further research in the field of alcohol-related dementia in the future.

One author of the study is Stephan Listabarth.

The study is published in the leading journal Alzheimer’s and Dementia.

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