Post by Admin on Jul 8, 2021 18:22:27 GMT
Chronic Stress, Genetics May Raise Alzheimer's Risk
www.medscape.com/viewarticle/954355
A review of human and animal epidemiological studies found that long-term stress and genetic factors may act through the hypothalamic-pituitary-adrenal (HPA) axis a pathway in the brain that mediates stress responses to contribute to the development of Alzheimer's disease. The researchers also proposed a mechanism to account for how genetic factors may affect HPA axis reactivity and lead to inflammation, which is a core component of neurodegeneration.
"Chronic stress can impact the way immune cells in the brain function and increase inflammation. Genetic variants within that stress response can further affect the function of immune cells," lead author Ayeisha Milligan Armstrong, a PhD candidate at Curtin Health Innovation Research Institute in Perth, Australia, said in an interview.
The findings were published online June 22 in Biological Reviews).
Research has found that long-term stress during early and mid-life is increasingly associated with cognitive decline and neurodegeneration. There is already evidence to suggest that chronic stress is a risk factor for the "sporadic" or late-onset subtype of Alzheimer's disease.
A Cascade of Events
Stress activates the HPA, which in turn regulates bodily levels of cortisol, a glucocorticoid stress hormone. Increased levels of cortisol are frequently observed in patients with Alzheimer's disease and "make a major contribution to the disease process," the authors wrote. For example, the hippocampus – a part of the brain involved in processing and forming memories – has numerous glucocorticoid receptors and is "therefore particularly sensitive to the effects of glucocorticoids." However, the molecular mechanisms involved remain poorly understood.
"There is an intimate interplay between exposure to chronic stress and pathways influencing the body's reaction to such stress," senior author David Groth, PhD, said in a statement. Groth is an associate professor at Curtin University in Perth, Australia.
There is variation between individuals with regard to how sensitive they are to stress and glucocorticoid responses. Environmental factors such as stress are thought to be at least partly responsible, as are genetic factors such as genetic polymorphisms and epigenetics. "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," Groth said.
www.medscape.com/viewarticle/954355
A review of human and animal epidemiological studies found that long-term stress and genetic factors may act through the hypothalamic-pituitary-adrenal (HPA) axis a pathway in the brain that mediates stress responses to contribute to the development of Alzheimer's disease. The researchers also proposed a mechanism to account for how genetic factors may affect HPA axis reactivity and lead to inflammation, which is a core component of neurodegeneration.
"Chronic stress can impact the way immune cells in the brain function and increase inflammation. Genetic variants within that stress response can further affect the function of immune cells," lead author Ayeisha Milligan Armstrong, a PhD candidate at Curtin Health Innovation Research Institute in Perth, Australia, said in an interview.
The findings were published online June 22 in Biological Reviews).
Research has found that long-term stress during early and mid-life is increasingly associated with cognitive decline and neurodegeneration. There is already evidence to suggest that chronic stress is a risk factor for the "sporadic" or late-onset subtype of Alzheimer's disease.
A Cascade of Events
Stress activates the HPA, which in turn regulates bodily levels of cortisol, a glucocorticoid stress hormone. Increased levels of cortisol are frequently observed in patients with Alzheimer's disease and "make a major contribution to the disease process," the authors wrote. For example, the hippocampus – a part of the brain involved in processing and forming memories – has numerous glucocorticoid receptors and is "therefore particularly sensitive to the effects of glucocorticoids." However, the molecular mechanisms involved remain poorly understood.
"There is an intimate interplay between exposure to chronic stress and pathways influencing the body's reaction to such stress," senior author David Groth, PhD, said in a statement. Groth is an associate professor at Curtin University in Perth, Australia.
There is variation between individuals with regard to how sensitive they are to stress and glucocorticoid responses. Environmental factors such as stress are thought to be at least partly responsible, as are genetic factors such as genetic polymorphisms and epigenetics. "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," Groth said.