A review published in the journal Alzheimer and Dementia has shone a spotlight on stress, stress physiology and Alzheimer disease outcomes. This review, which adopted a narrative, state-of-the-art synthesis approach, collated epidemiological, neuroendocrine and neuropathological evidence linking stress to Alzheimer’s disease. In doing so, it demonstrates why stress is important as both a risk factor and disease modifier and highlights the implications for future research, clinical trial design, and interventions.
In terms of being a risk factors, chronic stress, defined as repeated acute stress, or intense traumatic events that exceed an individual’s threshold to change and adapt, can lead to long-term adverse health effects. Research shows that people who experience long-term stress, loneliness, social isolation, childhood adversity, trauma, or conditions such as Post-traumatic stress disorder (PTSD) tend to have a higher risk of developing dementia, including Alzheimer's disease. Stress, when measured by biological markers like cortisol (a stress hormone), heart-rate, blood pressure, and brain imaging has been linked to an increased likelihood of developing Alzheimer's later in life.
Chronic stress may contribute to the biological processes involved in Alzheimer's disease by activating hormonal and nervous-system pathways that, when overused, can damage brain regions important for memory and thinking. Long-term activation of stress chemicals such increase inflammation and have been linked to processes thought to drive Alzheimer’s disease (amyloid plaques and tau tangles). Indeed, some of the brain structures involved in the stress response are also among the first affected by Alzheimer's, suggesting a close connection. In totality, this article suggests a need to monitor stress levels and implement strategies to mitigate stress if possible.
More information on this study is available here:
https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.71542?utm_medium=article&utm_source=researchgate.net
