Jet Lag, Dementia May Be a Thing of the Past, According to New Research

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Jet lag, along with dementia and other sleep disorders, may be a thing of the past, since scientists recently discovered the gene that causes the condition.

The Body’s Internal Clock

Every cell in the body has a clock, so to speak, with a multitude of proteins that ebb and flow over the course of 24 hours. The master “clock”, or the nucleus responsible for establishing each cell’s rhythm and keeping them in sync is the suprachiasmatic nucleus (SCN). The close interaction of the neurons in the SCN in combination with human exposure to light and darkness generally allows people to keep the same schedule day to day.

However, this interaction makes the cells resistant to change and often leads to jet lag.

Research on Lhx1

Researchers at the Salk Institute for Biological Studies addressed the problem by adjusting the day-night cycle of mice by 8 hours, and found that mice with little or no of the Lhx1 gene adjusted much faster to the shift than normal mice.

Lhx1 is known for controlling waking and sleeping patterns. The gene could also help control dementia or sleeping disorders, and be especially useful for shift workers.

Researchers also found that mice with little of the Lhx1 gene exhibited reduced activity of the vasoactive intestinal peptide (Vip) gene, which is regulated by Lhx1.

“This approach helped us to close that knowledge gap and show that Vip is a very important protein, at least for the suprachiasmatic nucleus,” Professor Satchidananda Panda, the study’s author, said. “It can compensate for the loss of Lhx1.”

In short, suppressing Lhx1 and reducing Vip prevents cells in the SCN from communicating, meaning they become unsure what time of day they should be operating. If researchers continue to study the gene, jet lag could soon become a condition of the past.

Additionally, the gene may be able to help researchers combat conditions like dementia, which Panda explained is often influenced by sleep disturbances.

Source: DailyMail

 
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