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Why You Could be Stressing Your Way to Alzheimer's Disease

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Why You Could be Stressing Your Way to Alzheimer's Disease about undefined
Short term stresses are part of everyday life; nothing to be concerned about. However, chronic, unrelenting stress is something else, and has long been recognized as a risk factor for Alzheimer's disease. Yet researchers remain unclear as to why this is so. After reviewing all the existing research, scientists from Australia have come up with an answer that links stress hormones to immune cells and inflammation that can trigger memory loss. Here’s the story and what it means for you... Stress is not an easy subject to investigate because it has different causes and people experience stress in different ways. It's also difficult to separate the effects of stress from other health issues. For example, anxiety, depression and insomnia are all linked to dementia but also go hand in hand with stress, so are these conditions driving the increased risk for dementia or is it some other aspect of stress? In spite of the difficulties, attempts have been made to measure the stress response and untangle it from other factors, but with no clear answers. The current view is that prolonged stress may play a role in dementia development and progression but isn't necessarily causing the condition. Researchers at Curtin University in Perth recently carried out a thorough review of the connection between chronic stress and Alzheimer's disease, publishing their findings in the journal Biological Reviews in June. If they’re right in their assessment, we urgently need to find ways to combat stress.

Genetic and Environmental Factors 

The researchers begin their report by reminding us that the body's central stress response system is the hypothalamic pituitary adrenal (HPA) axis. In response to stress a cascade of events take place that are regulated by this axis and that culminate in the release of glucocorticoids, including the stress hormone, cortisol. High levels of cortisol have been linked to memory loss and brain shrinkage. They’re also commonly found in Alzheimer's patients. In the population at large, people vary in their sensitivity to glucocorticoids and stress responses for both genetic and environmental reasons. These differences, the researchers write, "could ultimately impact an individual's risk of Alzheimer's disease." Genetic and environmental factors, they propose, prime the glucocorticoids to induce the microglia, the brain's immune cells, to become pro-inflammatory and, they write, "promote a neurotoxic environment resulting in neurodegeneration." For these reasons it's important to identify genetic factors, engage in stress management and take into account the potential risks associated with the common use of glucocorticoids to treat a wide variety of illnesses.

New Reason to Exercise, Relax and Laugh 

Lead author and expert in the molecular mechanisms of Alzheimer’s disease, associate professor David Groth, commented on their research, saying, "What we know is that chronic stress does affect many biological pathways within our body. There is an intimate interplay between exposure to chronic stress and pathways influencing the body's reaction to such stress. "Genetic variations within these pathways can influence the way the brain's immune system behaves leading to a dysfunctional response. In the brain, this leads to a chronic disruption of normal brain processes, increasing the risk of subsequent neurodegeneration and ultimately dementia. “There remains a need for a greater understanding of how genetic factors influence reactivity to cortisol and chronic stress and may interact with specific cell types, such as microglia, to promote Alzheimer’s.” While we can’t change certain genetic factors we can certainly focus on reducing stress through physical exercise, developing good sleep habits, scheduling time for relaxation and mindfulness exercises, and engaging in activities that regularly bring us joy and laughter.
  1. https://www.emedicinehealth.com/script/main/art.asp?articlekey=261338
  2. https://onlinelibrary.wiley.com/doi/10.1111/brv.12750 

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