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Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
White matter functional and structural alterations of spinocerebellar ataxia type 3: A longitudinal MRI study
Jingyi Tang1, Wu Xing1, Dongcui Wang1
1Department of Radiology, Xiangya Hospital of Central South University, Changsha, 410008, China.
Abstract:
Widespread white matter (WM) microstructural abnormalities have been reported in patients with spinocerebellar ataxia type 3 (SCA3) using diffusion tensor imaging (DTI), whereas the ability of DTI to detect WM degeneration over short-term period remains insufficiently explored. Additionally, WM dysfunction remains entirely unknown in this disease. This study aims to investigate WM structural and functional alterations in SCA3, and provide promising progression biomarkers for short-term clinical trials. DTI and resting-state functional magnetic resonance imaging data of 52 SCA3 patients and 56 healthy controls (HCs) were collected at baseline. After a mean follow-up of 1 year, MRI scans were performed on a subset of 28 SCA3 patients. Compared with HCs, widespread WM structural and functional abnormalities were observed in patients with SCA3. Between-group differences of both structural and functional MR metrics showed remarkable similarities, with large differences located in pons and corticospinal tracts, involving cerebellar WM, cerebellar and cerebral peduncles, medial lemniscus and bilateral posterior limb of internal capsule (PLIC). The longitudinal analysis further showed decreased ALFF in the right PLIC and increased mean diffusivity in the left inferior cerebellar peduncle and right medial lemniscus over time in SCA3 patients. These findings emphasized that pons and the CST were the most vulnerable WM areas in SCA3, and have the potential to become therapeutic targets of SCA3 for upcoming interventional trials. In addition, both DT metrics and WM ALFF were efficient progression biomarkers for SCA3 even in short-term period.
Insights
Spinocerebellar ataxia type 3 (SCA3) shows widespread white matter (WM) abnormalities. Diffusion tensor imaging (DTI) and functional MRI reveal structural and functional changes, identifying potential biomarkers for short-term clinical trials.
Area of Science:
- Neuroimaging
- Neurology
- Biomarkers
Background:
- Spinocerebellar ataxia type 3 (SCA3) is characterized by white matter (WM) microstructural abnormalities.
- Previous studies using diffusion tensor imaging (DTI) have shown these abnormalities, but short-term changes and functional WM alterations remain understudied.
- Understanding WM dysfunction is crucial for developing effective treatments for SCA3.
Purpose of the Study:
- To investigate structural and functional alterations in WM in SCA3 patients.
- To identify potential progression biomarkers for short-term clinical trials in SCA3.
- To explore the short-term changes in WM integrity and function over a one-year period.
Main Methods:
- Utilized DTI and resting-state functional MRI (rs-fMRI) on 52 SCA3 patients and 56 healthy controls (HCs) at baseline.
- Conducted follow-up MRI scans on a subset of 28 SCA3 patients after a mean of one year.
- Analyzed both structural (DTI metrics) and functional (ALFF from rs-fMRI) WM changes.
Main Results:
- SCA3 patients exhibited widespread structural and functional WM abnormalities compared to HCs.
- Abnormalities were notably concentrated in the pons and corticospinal tracts (CST), including cerebellar WM, peduncles, medial lemniscus, and posterior limb of the internal capsule (PLIC).
- Longitudinal analysis revealed decreased ALFF in the right PLIC and increased mean diffusivity in the left inferior cerebellar peduncle and right medial lemniscus over one year.
Conclusions:
- The pons and CST are the most vulnerable WM areas in SCA3, representing potential therapeutic targets.
- DTI metrics and WM ALFF are effective progression biomarkers for SCA3, even over short observation periods.
- These findings support the use of neuroimaging biomarkers for monitoring disease progression and treatment efficacy in SCA3 clinical trials.

