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Amyotrophic lateral sclerosis ALS is a progressive neurodegenerative disease characterized by motor neuron cell loss, muscular atrophy, and a shortened life span. Survival is highly variable, as some patients die within months, while others live for many years.

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Exposure to stress or the development of a nonoptimal stress response to disease might account for some of this variability. We show in the SOD1 G93A mouse model of ALS that recurrent exposure to restraint stress led to an earlier onset of astrogliosis and microglial activation within the spinal cord, accelerated muscular weakness, and a significant decrease in median survival vs.

Moreover, during normal disease course, ALS mice display a cacostatic stress response by developing an aberrant serum corticosterone circadian rhythm. Interestingly, we also found that higher corticosterone levels were significantly correlated with both an earlier onset of paralysis males: These results suggest that stress is capable of accelerating disease progression and that strategies that modulate glucocorticoid metabolism might be a viable treatment approach for ALS.

Disease progression in a mouse model Rev obanion sex charges northeast ohio amyotrophic lateral sclerosis: Amyotrophic lateral sclerosis ALS is a fatal neurodegenerative disorder characterized Rev obanion sex charges northeast ohio a selective loss of motor neurons in the motor cortex, brain stem, and spinal cord.

Although death typically occurs within 3—5 yr from diagnosis, some patients die within months, while others live for many years 1.

The reason for this wide variation in patient survival remains unclear. Several lines of evidence suggest that differences in exposure to stressful stimuli or the extent to which the neuroendocrine stress response system is activated following homeostatic disruption might account for some of the observed variability.

Interestingly, epidemiological studies indicate that individuals who have been repeatedly exposed to psychological and physical stress e. However, it remains to be determined whether a causal relationship truly exists between a patient's level of stress and the rate at which the disease progresses. Stress is defined as an internal or external adverse threat to homeostasis that is either real or perceived to be so 6 — 8.

Protection against acute stress or reestablishment of homeostasis is achieved by a complex repertoire of physiological increased oxygenation and energy delivery to the brain, heart, and skeletal muscles and behavioral inhibition of nonadaptive functions, such as eating, growth, and reproduction adaptive responses 6 — 8.

These adaptive responses are thought to exert their effects in an inverted U-shaped dose—response curve Fig.

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Healthy homeostatic or eustatic stress responses are achieved in the central, optimal range of the curve, whereas stress responses that have the potential to initiate multiple adverse effects leading to a state known as allostasis or cacostasis occur on either side of the curve 67. Principal effectors of the stress response system include glucocorticoids cortisol in humans, corticosterone in rodentswhich are regulated by the hypothalamic—pituitary—adrenal axis, and norepinephrine and epinephrine, catecholamines that are regulated by the systemic and adrenomedullary sympathetic nervous systems 9 When these mediators, which are meant to be secreted in a quantity- and time-limited manner, are released chronically, the organism is exposed to a series of negative behavioral Rev obanion sex charges northeast ohio somatic consequences i.

Stress response system exerts its effects in an inverted U-shaped dose response modified from ref.


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