A gene linked to job-related exhaustion in shift workers also increases the risk of Alzheimer’s

Melatonin receptor type 1A gene linked to Alzheimer’s disease in old age.

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Alzheimer’s disease is a memory disorder that causes the brain to deteriorate. One of its risk factors is disruption of sleep and the circadian rhythm. Lack of sleep and disruption of the circadian rhythm are common among shift workers. Tolerance to the negative effects of shift work varies between individuals and is partially linked to intrinsic genetic factors.

According to a new Finnish study, a variety in the melatonin receptor 1A (MTNR1A) gene is connected to the danger of Alzheimer’s in the elderly. A similar research group has already exhibited that the same genetic variation lessens resilience to move work among the working-age populace.

The study suggests that the MTNR1A gene variation along with Alzheimer’s diagnosis is connected to mind sores noticeable in posthumous brain tissues. Likewise, when the outflow of the MTNR1A gene was diminished in the cell culture, beta-amyloid protein normal for Alzheimer’s disease begun to gather.

The previous study also discovered the same gene variation that predisposes to shift work fatigue is associated with lower levels of the MTNR1A gene expression in the brain.

Lic. Med Sonja Sulkava from the National Institute for Health and Welfare (THL) said, “The finding of a common risk gene for both job-related exhaustion in shift workers and Alzheimer’s disease doesn’t directly mean that shift work would predispose to Alzheimer’s disease. However, the combination of genetic predisposition and a lifestyle that disrupts the circadian rhythm can increase the risk of Alzheimer’s disease. Another possible interpretation is that the brain dysfunctions related to Alzheimer’s disease impair the tolerance to shift work decades before the onset of the clinical disease.”

The study led by Professor Tiina Paunio, University of Helsinki and National Institute for Health and Welfare (THL), Finland said, “Even though our results demonstrate a new molecule-level connection between the tolerance to shift work and incipient Alzheimer’s disease, the now discovered genetic variation has a minimal effect on the individual level and it can’t be used to risk assessment or prediction.”

The exploration accomplices comprised of more than 85-year-olds living in Vantaa and more than 75-year-olds living in Kuopio and of Alzheimer patients and healthy controls living in Eastern Finland. The connection could be found in elderly partners yet not in the more youthful patient and control associates.

The study is published in the SLEEP journal.

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