Summary: A new study reveals that high levels of cortisol in quarantine are linked to an increase in the amyloid deposit of the brain – a key marker of Alzheimer’s disease, especially in post -menopausal women. The researchers followed 305 individuals in good cognitive health over 15 years and discovered that high cortisol predicted the amyloid accumulation later in life, but only in women who had crossed menopause.
The results suggest that hormonal changes can amplify the harmful effects of cortisol on brain health. No similar relationship has been found in men or with the Tau protein, another Alzheimer’s marker.
Key facts:
- Specific gender risk: Cortisol of big life in the big life predicted the risk of Alzheimer’s only in menopausal women.
- Amyloid link: Cortisol levels were associated with an increase in amyloid accumulation, not Tau.
- Prevention potential: The results suggest that early stress reduction and hormone -based strategies could reduce the risk of Alzheimer’s.
Source: Ut San Antonio
Can stress lead to Alzheimer’s disease? He can in post-Menopause women, a study led by the Center for Health Sciences at the University of Texas in San Antoino (UT Health San Antonio).
The data analysis of 305 cognitively unarmed participants in Framingham Heart Study, a long-term and undergoing community cohort study on Framingham, Massachusetts residents, scientists have discovered that high levels of stress hormony in people in living areas are linked to an increase in the amyloid deposit in post-men.
Amyloids are proteins that have folded incorrectly, preventing biological function, forming deposits in tissues and organs, and involved in Alzheimer’s disease.
By comparing the cortisol levels of the quarantine at the start of a period of 15 years with indicators of the disease at the end, the researchers were able to determine that these levels could serve as a biomarker of Alzheimer’s disease, with particular attention to the differences between the sexes and the state of menopause.
No significant association has been observed in men or with the TAU load, referring to the Tau protein which contributes to neuronal dysfunction and death.
“The results highlight the importance of identifying early risk factors when the biomarkers are detectable but that cognitive disorders are absent,” said Arash Salardini, MD, associate professor of cognitive and behavioral neurology with the Glenn Biggs Institute for Alzheimer and Neurodegenerative Diseases in Ut Health Antonio.
Salardini is the first author of the study entitled “High serum cortisol associated with an early detected increase in the amyloid brain deposit in Alzheimer’s disease imaging biomarkers in menopausal women: The Framingham Heart Study”, published on April 24 in April 24 Alzheimer’s and dementia: The newspaper of the Alzheimer’s association.
Other authors are also with Ut Health San Antonio, as well as the San Antonio of the Public Health School of the University of Texas; Cardiac study of Framingham of the National Institute of the Heart, Lungs and Blood of the National Institutes of Health; University of Boston; Gonzaba Medical Group, San Antonio; University of Galway, Ireland; CEDARS-SINAI medical center; Massachusetts General Hospital / Harvard Medical School; New York University of Medicine School; Brigham and Women’s Hospital; University of Yale; And the University of California in Davis.
“Our work shows that the consideration of sex and hormonal status in understanding the pathogenesis of Alzheimer’s disease is important, and suggests that the reduction of stress and hormonal interventions can be promising Alzheimer’s prevention, in particular in women at risk,” said Sudha Seshadri, founding director of the Biggs Institute and the main author of the study.
Target risk factors early
The study notes that “sporadic” Alzheimer’s disease is the main cause of cognitive decline in the elderly. Which has an prolonged asymptomatic phase of amyloid beta accumulation, the main component of amyloid plates, finally triggering a progressive cognitive decline.
Recognizing that these biological changes are already well established when symptoms emerge, effective early interventions must target risk factors for Alzheimer’s disease during preclinical stages.
However, despite significant progress in understanding how the disease affects normal biological processes of the body, more than half of the overall risk has remained unexplained, stressing the critical need to identify additional risk factors that can be targeted during the preclinical stage.
A promising investigation line focuses on cortisol, an essential steroid hormone for cellular homeostasis, or balance, and the response to stress.
Genetic studies had identified mutations in glucocorticoids or steroid hormones that have anti-inflammatory and immunosuppressive effects, signaling pathways that increase sensitivity to Alzheimer’s disease.
In addition, several transversal and longitudinal studies have reported that higher blood cortisol levels are linked to an increased probability of developing the disease.
To fill the gaps and inconsistencies through these studies, the researchers led by UT Health San Antonio have conducted a longitudinal analysis using data from the third generation cohort of the study of the Coeur Framingham, which dates from 1948 and is now led by the National Institute of the Heart, lungs and blood of the National Institute of Health.
They evaluated the relationship between serum cortisol rates in the 305 individuals of the average non -altered cognitively age – 48.5% of women, with an average age of 39.6 years – and amyloid / tau charges about 15 years later using imaging by computed tomography (PET). And they carried out adjusted multivariable regression analyzes for confusion factors.
All this has enabled them to study the impact of cortisol at an anterior stage of the pathogenesis of Alzheimer’s disease, where interventions could be the most effective.
Given the neuroprotective effects of estrogen and testosterone, which reduce the deleterious impact of cortisol on neural tissue, they also explored the specific differences to sex, by focusing in particular on post-menopausic risk.
They hypothesized that the impact of cortisol on Alzheimer’s pathology would be more pronounced in women, in particular after menopause, in accordance with certain previous conclusions.
Indeed, they found that post-menopausal women with cortisol of the high quarantine run an increased risk of Alzheimer’s disease, and that post-menopause hormonal changes can amplify the effects of cortisol on the amyloid.
“The longitudinal monitoring of our cohort will be crucial to determine whether these first amyloid changes result in clinical symptoms and to clarify the causal role of cortisol in the development of Alzheimer’s disease,” said Salardini.
About this news of research on Alzheimer’s disease
Author: Steven Lee
Source: Ut San Antonio
Contact: Steven Lee – Ut San Antonio
Picture: The image is credited with Neuroscience News
Original search: Open access.
“A high serum cortisol associated with an early increase detected of the amyloid brain deposit in biomarkers of imagery of Alzheimer’s disease in menopausal women: the study of the heart of Framingham” by Arash Salardini et al. Alzheimer’s and dementia
Abstract
High serum cortisol associated with an early detected increase in the amyloid deposit of the brain in imagery biomarkers of Alzheimer’s disease in menopausal women: Cardiac study of Framingham
INTRODUCTION
This study examines whether the quarantine cortisol levels predict the load of biomarkers of Alzheimer’s disease (AD) 15 years later, with particular attention to sexual differences and the menopausic state.
Methods
We have analyzed the data of 305 participants in the cardiac study of cognitively non -altered framingham (48.5% of women; average age: 39.6 ± 8.1 years). Seric cortisol has been classified as tertiles, with the amyloid (((((11C) GDP) and tau (((18F) flortucipiir) Imaging of positron’s emission tomography (TEP) led 15 years later. We have carried out adjusted multivariate regression analyzes for confusion factors, including the status of apolipoprotein E4 (APOE4).
RESULTS
The high cortisol of quarantine in living in life was in correlation with an increase in amyloid deposit, especially in menopausal women, mainly in the posterior, precopinus and frontal side regions (p
DISCUSSION
These results reveal that menopausal women with cortisol of the high quarantine run an increased risk of MA. The results highlight the importance of identifying early risk factors when the biomarkers are detectable but the cognitive disorders are absent.
