渡辺 宏久

INTRODUCTION: Progressive supranuclear palsy (PSP) involves midbrain structures, including the red nucleus (RN), an iron-rich region that appears as a high-contrast area on quantitative susceptibility mapping (QSM). RN may serve as a promising biomarker for differentiating parkinsonism. However, RN deformation in PSP remains elusive. This study aimed to evaluate RN deformation in PSP using coronal QSM images and compare them with those of Parkinson's disease (PD) and healthy controls (HC). METHODS: We evaluated the QSM images of 22 patients with PSP, 37 patients with PD, and 43 HC. We developed a grading system to assess RN deformation on coronal QSM images and classified them into three grades. The midbrain and RN volumes were extracted using distinct approaches, and their relationship with grading was investigated. For validation, coronal QSM images of 16 PSP patients from a different institution were assessed. RESULTS: In PSP, 59 % of the patients displayed a flattened RN of grade 3, which we termed a Rice-Grain Appearance. The volume reductions in midbrain and RN were associated with deformation. Differentiation based on the presence of this appearance yielded a specificity of 1.000 (CI: 1.000-1.000) and sensitivity of 0.591 (0.385-0.796) for distinguishing PSP from others. Secondary dataset also showed that 56 % of patients with PSP were classified as grade 3. CONCLUSION: In coronal QSM images, the flattened RN shape appears to be specific to PSP compared to PD and HC and may serve as a marker to help differentiate PSP in future clinical settings.

OBJECTIVES: Sudden death in multiple system atrophy (MSA) is caused by decreased serotonergic innervation, but there is no routine test method for this decrease. In addition to dopamine transporters, iodine-123-labelled N-(3-fluoropropyl)-2β-carbomethoxy-3β-(4-iodophenyl) nortropane (123I-FP-CIT) binds serotonin transporters (SERTs). We noted a binding potential to quantify the total quantity of 123I-FP-CIT binding to its receptors.Following Mintun's binding-potential concept, this study aimed to evaluate the relationship between the specific binding ratio (SBR) and total SERT tissue amount, but not SERT binding, and to develop an SBR imaging method to measure brain-stem SERT. We sought to establish a binding-potential imaging procedure using SBR images to examine differences in the brain-stem SERT distribution between healthy subjects and MSA patients. METHODS: Single-photon emission computed tomography (SPECT) and T1-weighted magnetic resonance (MR) images were aligned. The MR (T1) images were used to set a reference site for the occipital-lobe SBR in each subject, and measurements were made from the SPECT image at the same position. The pixel values and accumulation ratios compared with the occipital lobe were calculated, and a regional SBR distribution image was created. We identified areas with SERT accumulation above a certain level. RESULTS: The SERT accumulation site was visualised as an SBR value on MR images. The accumulation distribution (SERT distribution) on the SBR images significantly differed between the healthy subjects and patients with MSA. CONCLUSION: SERT accumulation was noted in the brain-stem region, indicating that SBR imaging was useful for viewing and quantifying SERT accumulation.

<jats:sec><jats:title>Background</jats:title><jats:p> Recent evidence suggests a link between glycoprotein non-metastatic melanoma protein B (GPNMB) and Parkinson's disease (PD) pathogenesis. Although elevated plasma GPNMB levels associated with disease severity have been reported in PD, cerebrospinal fluid (CSF) alterations remain elusive. </jats:p></jats:sec><jats:sec><jats:title>Objective</jats:title><jats:p> To explore CSF GPNMB alterations and its clinical significance in PD. </jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p> This study enrolled 118 sporadic PD patients and 40 controls. We examined the potential associations between CSF GPNMB levels and the clinical characteristics or biomarkers of neurodegenerative pathogenesis. </jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p> PD patients had higher CSF GPNMB levels than controls ( p = 0.0159). In the PD group, CSF GPNMB levels correlated with age (age at examination: r<jats:sub>s </jats:sub>= 0.2511, p = 0.0061; age at onset: r<jats:sub>s </jats:sub>= 0.2800, p = 0.0021) and the severity of motor and cognitive dysfunction (MDS-UPDRS III score: r<jats:sub>s </jats:sub>= 0.1998, p = 0.0347; Mini-Mental State Examination score: r<jats:sub>s </jats:sub>= −0.1922, p = 0.0370). After correcting for multiple comparisons, the correlation with age at onset remained significant. CSF GPNMB levels were also positively correlated with CSF soluble triggering receptor expressed on myeloid cells 2 (sTREM2) levels in both the PD ( r<jats:sub>s </jats:sub>= 0.3582, p &lt; 0.0001) and control ( r<jats:sub>s </jats:sub>= 0.4743, p = 0.0023) groups. Furthermore, multiple regression analysis revealed CSF sTREM2 level as the strongest determinant of CSF GPNMB levels in the PD group (t-value = 3.49, p = 0.0007). </jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p> Elevated CSF GPNMB levels, linked with age and microglial activation, may be a valuable marker for understanding the interplay between aging, neuroinflammation, and PD pathology. </jats:p></jats:sec>