It can be classified into three types : vascular dementia (VaD), Alzheimer’s disease (AD) with a vascular component, and vascular cognitive impairment, no dementia (VCIND). A major cause of VCI is a subcortical ischemic vascular disease (SIVD) or small vessel disease (SVD). A cerebral SVD/SIVD or cerebral microangiography is induced when blood circulation in arterioles is impaired. It can be easily distinguished by white matter lesions (WML) and lacunar infarcts. The Schaefer research aims to identify the changes in functional connectivity for SVD. Changes in functional connectivity in posterior cingulate cortex (PCC) and in the DMN are mentioned in the previous research. Schaefer 's study focuses mainly on the frontoparietal networks and their altering connectivity. The research involved 12 participants whose rs-fMRI, T1- and T2- weighted anatomical data were acquired. Patient whose age-related white-matter changes (ARWMC) score >2 and had SVD were chosen for the study. FSL, AFNI and SPM, were used in preprocessing of the rs-fMRI data. Eigenvector centrality, which a measure utilized in graph theory, connectivity was obtained. The results manifested connectivity decline in left ventromedial prefrontal cortex (vmPFC), bilateral midcingulate cortex (MCC) and right superior parietal lobe. An increase in functional connectivity was visualized in bilateral cerebellar regions I to VI. Further a correlation of WML score and Eigen value centrality map informed a decrease in connectivity in bilateral vmPFC, PCC, left supplementary motor area (SMA,) and right SPL. The results clearly explain that the WML present in the frontal and parietal areas of the participants provides verification that frontoparietal networks are disrupted in SVD. Further, a diminished connectivity was exhibited by the medial frontal cortex, because of the white matter hyperintensities. Some of
It can be classified into three types : vascular dementia (VaD), Alzheimer’s disease (AD) with a vascular component, and vascular cognitive impairment, no dementia (VCIND). A major cause of VCI is a subcortical ischemic vascular disease (SIVD) or small vessel disease (SVD). A cerebral SVD/SIVD or cerebral microangiography is induced when blood circulation in arterioles is impaired. It can be easily distinguished by white matter lesions (WML) and lacunar infarcts. The Schaefer research aims to identify the changes in functional connectivity for SVD. Changes in functional connectivity in posterior cingulate cortex (PCC) and in the DMN are mentioned in the previous research. Schaefer 's study focuses mainly on the frontoparietal networks and their altering connectivity. The research involved 12 participants whose rs-fMRI, T1- and T2- weighted anatomical data were acquired. Patient whose age-related white-matter changes (ARWMC) score >2 and had SVD were chosen for the study. FSL, AFNI and SPM, were used in preprocessing of the rs-fMRI data. Eigenvector centrality, which a measure utilized in graph theory, connectivity was obtained. The results manifested connectivity decline in left ventromedial prefrontal cortex (vmPFC), bilateral midcingulate cortex (MCC) and right superior parietal lobe. An increase in functional connectivity was visualized in bilateral cerebellar regions I to VI. Further a correlation of WML score and Eigen value centrality map informed a decrease in connectivity in bilateral vmPFC, PCC, left supplementary motor area (SMA,) and right SPL. The results clearly explain that the WML present in the frontal and parietal areas of the participants provides verification that frontoparietal networks are disrupted in SVD. Further, a diminished connectivity was exhibited by the medial frontal cortex, because of the white matter hyperintensities. Some of