Early Inflammatory Response To Stress

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Heterodynamic Context Exogenous threats can shape stress responses across the lifespan, and influences the rate of aging (ES-2014-aging). Environmental stressors include any factors that cause cell injury, such as heavy metals, radiation, heat exposure, reactive oxygen species, osmotic fluctuation, as well as social and psychological stressors (ES-2014). These trigger the stress response and related behavioral pathways through neural networks and interconnected neurohormonal and immune patterns. The capacity of human beings to learn about, imagine, remember, and anticipate stressful situations and their warning signs can create chronic states of vigilant arousal in the body. Besides, there are multiple individual differences that make some people more vulnerable to stress, where the identical stimuli cause exaggerated stress responses (ES-2014). Gene-environment interactions in PD Because of the low heritability of PD, more studies focusing on environmental exposures about the PD mechanism (AH-2012). Researchers may focus on both chemical hazards and physical hazards (AH-2012). Exposure to environmental factors or mutations in PD-associated genes of patients may cause mitochondrial dysfunction that ultimately results in PD. All of these share common linkages and influence each other greatly. Limiting the early inflammatory response will reduce further both elevated oxidative stress and microglial activation that are key to slowing the death of the neurons in the SNpc.

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