Comparison between sub-chronic and chronic sleep deprivation-induced behavioral and neuroimmunological abnormalities in mice: focusing on glial cell phenotype polarization.

In people with autoimmune disease, consistently not getting enough sleep reduces the effectiveness of immune system control and cellular repair processes.

In female mice, prolonged lack of sleep causes memory problems, increases inflammatory markers in brain cells, reduces neurotransmitter metabolism, and changes how amyloid precursor protein is processed. Short-term sleep loss does not produce these effects.

In female mice, prolonged lack of sleep changes how amyloid precursor protein is processed, increasing one fragment (sAPPβ) and decreasing another (sAPPα), which lowers the ratio between them; shorter periods of sleep loss do not produce this change.

In female mice, prolonged sleep loss leads to behavioral changes resembling depression, higher levels of PER2 protein, increased activation of inflammatory brain cells, and reduced levels of norepinephrine and serotonin, with longer sleep deprivation causing stronger effects.

In female mice, prolonged lack of sleep causes a measurable change in the BMAL-1 protein that regulates daily biological rhythms, but shorter periods of sleep loss do not produce this change.

In female mice, longer periods of sleep loss result in higher levels of inflammatory signaling molecules and greater activation of brain immune cells compared to shorter periods of sleep loss.