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Multiple studies in human and mouse models have shown that sleep disruption increases the risk of Alzheimer's disease (AD) by increasing the accumulation of disease-related proteins such as amyloid beta (Aβ) in the brain
TRN is static in AD
TRN is static in ADChin explained that when we sleep, TRN is generally more active than when we are awake
The authors first determined whether their AD mouse model would wake up more often during normal sleep times than mice without the disease
Static TRN is related to Aβ plaque load
Static TRN is related to Aβ plaque loadIn this AD mouse model, when these mice are about one month old, measurable Aβ levels begin to appear in the brain and begin to deposit Aβ plaques when they are about six months old
In summary, these findings indicate that sleep interruption in AD mice may affect the accumulation of Aβ protein in the brain that is involved in the progression of AD disease
In addition, Chin, Jagirdar and their colleagues analyzed the postmortem brain tissue of people with AD, mild cognitive impairment, or without these symptoms
Can reactivating TRN improve the condition?
Can reactivating TRN improve the condition?Using a chemical genetic system (a technique that allows people to chemically activate specific cells), the authors activated TRN neurons in a mouse model of AD
The authors pointed out that although this approach seems to improve sleep disruption and Aβ deposition in AD mouse models, not all sleep can be improved
Picture from Science Translational Medicine, 2021, doi:10.
Note: The original text has been deleted
Reference materials:
Rohan Jagirdar et al.