Yanbing Hou: Department of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Jing Yang: Department of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Chunyan Luo: Department of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Ruwei Ou: Department of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Wei Song: Department of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Wanglin Liu: Department of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Qiyong Gong: Department of Radiology, Huaxi MR Research Center (HMRRC), West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China. huaxigong@126.com.
Huifang Shang: Department of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China. hfshang2002@126.com.
To map functional connectivity (FC) patterns of early onset Parkinson's disease (EOPD) and late onset PD (LOPD) in drug-naïve early stage. MRI was used to assess atrophy and resting-state FC focusing on striatal subregions of EOPD and LOPD in two subgroups of 18 patients matched for disease duration and severity, relative to age- and sex- matched healthy controls. Compared with controls, both PD subgroups showed FC alterations in cortico-striatal and cerebello-striatal loops but with different patterns in resting state. EOPD patients showed widespread increased FC between striatum and sensorimotor cortex, middle frontal gyrus, superior and inferior parietal lobules, superior and inferior temporal gyri, and cerebellum. While LOPD patients were evidenced with increased FC in cerebello-striatal circuit and decreased FC between orbitofrontal gyrus and striatum. In addition, Unified Parkinson's Disease Rating Scale part III scores were negatively correlated with the increased FC between the caudate nucleus and sensorimotor cortex (r = -0.571, p = 0.013) in EOPD patients, while negatively correlated with the increased FC between the putamen and cerebellum (r = -0.478, p = 0.045) in LOPD patients, suggesting that increased FC is here likely to reflect compensatory mechanism. FC changes in EOPD and LOPD share common features and have differences, which may suggest that the responses to defective basal ganglia are different between the two subtypes. Improved insights into the onset-related subtypes of PD and its disruptive FC pattern will be valuable for improving our understanding of the pathogenesis of the disease.
