Scientists have found that sleep disturbances contribute to neurodegenerative diseases such as Alzheimer's disease. The results of the study were published in the journal Science Translational Medicine.

During the experiment, the researchers used wild-type mice and a mouse model of cerebral amyloidosis 5xFAD, which were subjected to chronic sleep deprivation. 5xFAD mice are characterized by the accumulation of amyloid plaques in the brain tissue - accumulations of pathogenic proteins that are considered a sign of Alzheimer's disease.

The humanized mouse model of 5xFAD expresses either a human gene variant known as the generic TREM2 variant, or a trigger receptor expressed on type 2 myeloid cells, or another variant that increases the risk of plaque accumulation. The scientists found that sleep deprivation increased TREM2-associated plaque accumulation compared to mice with normal sleep cycles.

As the authors write, sleep deprivation not only increased TREM2-dependent beta-amyloid plaque deposition, but also induced microglia (supporting brain tissue) reactivity that was independent of the presence of amyloid. Sleep deprivation alters the metabolic ability to cope with the energy demands of prolonged wakefulness, leading to further deposition of beta-amyloid.