Stress-induced decrease in resilience receptors may develop psychiatric disorders.

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The term “stress resilience” has become more common in medical biology papers in the last decade or so. It appears to be related not only to the development of neuropsychiatric disorders but also to exacerbations of Alzheimer’s disease and post-stroke neurodegeneration, and its detailed molecular pathology is expected to be elucidated for the treatment of neurological diseases. Fractalkine signaling is a signal involved in the immune response of microglia that affects stress resilience. Microglia express an fractalkine receptor, CX3CR1, and exchange signals with ligand-expressing neurons and other cells. The amount and form of the ligand fractalkine can inflect the stimulation of microglia and modulate its effects, ultimately modifying brain and nerve functions. Changes in CX3CR1 expression in microglia have been reported often, and it is generally accepted that its expression is altered by various stimuli, which may also occur in human diseases. Unfortunately, however, there is currently no clear direction as to whether this variation is uniformly good or bad for certain conditions. Nonetheless, this also being the case in humans, if we can prove beneficial changes in CX3CR1 for each individual disease by adjusting the life environment outside of clinical treatment, such as diet and exercise, then we may be able to acquire beneficial stress resilience through fractalkine signaling.

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