Publications by authors named "Jordan E. Tanley"
Background: The location of proposed brain MRI markers of small vessel disease (SVD) might reflect their pathogenesis and may translate into differential associations with cognition. We derived regional MRI markers of SVD and studied: (i) associations with cognitive performance, (ii) patterns most likely to reflect underlying SVD, (iii) mediating effects on the relationships of age and cardiovascular disease (CVD) risk with cognition.
Method: In 891 participants from The Multi‐Ethnic Study of Atherosclerosis, we segmented enlarged perivascular spaces (ePVS), white matter hyperintensities (WMH) and microbleeds (MBs) using deep learning‐based algorithms, and calculated white matter (WM) microstructural integrity measures of fractional anisotropy (FA), trace (TR) and free water (FW) using automated DTI‐processing pipelines.
Background: Little is known about how plasma Alzheimer’s disease (AD) biomarkers relate to neuroimaging biomarkers of cerebral small vessel disease (cSVD) in the context of neurodegeneration and AD pathology in late life.
Method: This cross‐sectional study included 251 Multi‐Ethnic Study of Atherosclerosis (MESA) Exam 6 participants with plasma AD biomarkers (Aβ42/Aβ40, GFAP, NfL, p‐tau181, p‐tau217, p‐tau231; Quanterix SIMOA), MRI (neurodegeneration and cSVD), PiB (amyloid) PET, and UDSv3‐based adjudicated cognitive status (69% cognitively normal, 27% MCI, 4% probable dementia) data at the Wake Forest site. Multivariable models examined relationships among cognitive status, plasma, and neuroimaging biomarkers (covariates: age, education, race, gender, smoking status, kidney function [eGFR], APOE‐ε4, BMI; significance at p<.
Background: Vascular disorders are proposed as modifiable risk factors for dementia; yet, physiologic mechanisms connecting vascular disorders to cognitive impairment remain unknown. We examined subclinical cardiovascular measures to determine which predict global cognitive decline and domain specific cognitive impairment and point to potential pathways linking subclinical vascular disease and dementia.
Methods: MESA includes a diverse cohort of 6,814 participants free from clinical cardiovascular disease with follow‐up over 6 clinical examinations and annual follow‐up calls.
Background: Vascular risk factors captured in midlife represent modifiable features of cardiovascular disease (CVD), stroke, dementia, and dementia‐related neuropathology. Subclinical measures of CVD may help identify specific structural and function aspects underlying vascular contributions to cognitive impairment and dementia over and above conventional dementia risk scores.
Method: The MESA study followed a diverse cohort of 6,814 adults aged 45‐84 years over 6 clinical examinations and annual follow‐up calls since baseline, 2000‐2002.
Background: Stiffening of the large elastic arteries is an emerging age‐related risk factor for Alzheimer’s disease (AD) and related dementia (ADRD). Arterial stiffness is associated with pathological changes underlying AD/ADRD, and total arterial stiffness (T‐PWV) can be subdivided into two main mechanisms. Structural stiffening (S‐PWV) is due to intrinsic remodeling of the artery wall, and load‐dependent stiffening (LD‐PWV) is due to increased blood pressure without intrinsic changes to the artery wall.
View Article and Find Full Text PDFBackground: The location of proposed brain MRI markers of small vessel disease (SVD) might reflect their pathogenesis and may translate into differential associations with cognition. We derived regional MRI markers of SVD and studied: (i) associations with cognitive performance, (ii) patterns most likely to reflect underlying SVD, (iii) mediating effects on the relationships of age and cardiovascular disease (CVD) risk with cognition.
Method: In 891 participants from The Multi‐Ethnic Study of Atherosclerosis, we segmented enlarged perivascular spaces (ePVS), white matter hyperintensities (WMH) and microbleeds (MBs) using deep learning‐based algorithms, and calculated white matter (WM) microstructural integrity measures of fractional anisotropy (FA), trace (TR) and free water (FW) using automated DTI‐processing pipelines.
Background: Little is known about how plasma Alzheimer’s disease (AD) biomarkers relate to neuroimaging biomarkers of cerebral small vessel disease (cSVD) in the context of neurodegeneration and AD pathology in late life.
Method: This cross‐sectional study included 251 Multi‐Ethnic Study of Atherosclerosis (MESA) Exam 6 participants with plasma AD biomarkers (Aß42/Aß40, GFAP, NfL, p‐tau181, p‐tau217, p‐tau231; Quanterix SIMOA), MRI (neurodegeneration and cSVD), PiB (amyloid) PET, and UDSv3‐based adjudicated cognitive status (69% cognitively normal, 27% MCI, 4% probable dementia) data at the Wake Forest site. Multivariable models examined relationships among cognitive status, plasma, and neuroimaging biomarkers (covariates: age, education, race, gender, smoking status, kidney function [eGFR], APOE‐e4, BMI; significance at p<.
Staging amyloid-beta (Aβ) pathophysiology according to the intensity of neurodegeneration could identify individuals at risk for cognitive decline in Alzheimer's disease (AD). In blood, phosphorylated tau (p-tau) associates with Aβ pathophysiology but an AD-type neurodegeneration biomarker has been lacking. In this multicenter study (n = 1076), we show that brain-derived tau (BD-tau) in blood increases according to concomitant Aβ ("A") and neurodegeneration ("N") abnormalities (determined using cerebrospinal fluid biomarkers); We used blood-based A/N biomarkers to profile the participants in this study; individuals with blood-based p-tau+/BD-tau+ profiles had the fastest cognitive decline and atrophy rates, irrespective of the baseline cognitive status.
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