Background: The primary aim of the current analysis was to evaluate the cumulative effect of different social determinants of health (SDoH) factors on vascular burden, cognition, and physical functioning.
Method: We conducted a secondary data analysis of the MIDUS 2 cross-sectional study. Participants were ages 55 and above. Measures derived from the Framingham Stroke Risk Profile, Brief Test of Adult Cognition by Telephone, and MOS-36 were used to represent vascular burden, cognition, and intermediate activities of daily living, respectively. SDoH variables included education, income, health insurance, stress, and support from family and friends. Associations were evaluated using composite-based structural equation model (c-SEM) embedded in an overall.
Result: Among cognitively normal adults (N = 568; mean age = 64.6), higher education, less stress, and higher income significantly contributed to the SDoH composite. Better standing in SDoH was associated with better physical functioning (beta = -0.21, p<0.001) and higher cognition (beta = 0.54, p<0.001). Significant direct effects of SDoH on vascular burden (beta = -0.12, p<0.05) and cognition (beta = 0.51, p<0.001), and of vascular burden on cognition (beta = -0.28, p<0.001) were found. Mediation analysis indicated that the unique effects of SDoH on cognition remained significant after controlling for vascular burden (beta = 0.04, p<0.05). After accounting for vascular burden and cognition, SDoH did not have a significant unique effect on physical functioning.
Conclusion: Our results support the disablement process that suggests that factors outside of the disease model (like SDoH factors) impact both the underlying diseases that lead to physical and functional limitation, all of which are associated with dementia/cognitive decline.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1002/alz.088011 | DOI Listing |
Alzheimers Dement
December 2024
Mass General Institute for Neurodegenerative Disease, Charlestown, MA, USA.
Background: Some individuals can tolerate the presence of Alzheimer disease neuropathologic changes (ADNC) (e.g., plaques and tangles) without developing dementia.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Departments of Neurology, Psychiatry, and Epidemiology, Gertrude H. Sergievsky Center, The Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Background: Cardio and cerebrovascular risk factors (CVRFs) increase the risk of cerebrovascular disease and clinical Alzheimer's Disease (AD), and over 70% of the patients with AD coincident cerebrovascular pathology. We previously found that FMNL2 interacts with a burden score of hypertension, diabetes, heart disease, and body mass index (BMI) by altering the normal astroglial-vascular mechanisms that underly amyloid clearance. Stroke, defined by history of a clinical stroke or brain imaging, is a moderately robust risk factor for AD and dementia.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of São Paulo Medical School, São Paulo, Brazil.
Background: Clinicopathological studies suggest a role of minor cerebrovascular changes in the cognitive decline of individuals with a low neurodegenerative burden. However, it remains unclear whether small vascular brain lesions can impact cognition in middle aging individuals. Additionally, recent clinicopathological studies have shown that even a low Alzheimer's disease (AD) neuropathological burden can significantly impact neuropsychiatric function.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Pittsburgh, Pittsburgh, PA, USA.
Background: Vascular cognitive impairment/dementia (VD) is the second most prevalent cause of dementia following Alzheimer's disease (AD). VD is characterized by the progression of white matter hyperintensity burden (WMH) and associated neurodegeneration. GFAP, a biomarker for reactive astrogliosis, is associated with Aβ pathology and mediates tau-pathology in preclinical AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Indiana University School of Medicine, Stark Neurosciences Research Institute, Department of Neurology, Indianapolis, IN, USA.
Anti-amyloid immunotherapy holds great promise for our patients and their families as the first disease-modifying therapy for the treatment of Alzheimer's disease (AD) to be approved. Positive clinical trials for lecanamab and donanemab showed significant and rapid lowering of brain amyloid burden and a significant slowing of cognitive decline. Amyloid-related imaging abnormalities (ARIA) in the form of vasogenic edema (ARIA-E) and micro - and macro- hemorrhages (ARIA-H) remain the major obstacle to broad use of these agents.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!