Kyoto University · Medicine
Professor Kazuto Tsukita's research lab focuses on the molecular and cellular mechanisms underlying neurodegenerative diseases, particularly Parkinson’s disease (PD), with an emphasis on proteinopathies, neuroinflammation, and cellular junction dynamics. The lab investigates pathological biomarkers such as α-synuclein deposits and cerebrospinal fluid proteomes using advanced proteomics and machine learning, aiming to improve early diagnosis and disease staging. Additionally, the lab explores the role of cellular junctions—especially the apical junctional complex—and their regulation by signaling molecules like AMPK and phase-separated proteins such as Cobl in maintaining epithelial and neural homeostasis. A key theme is the interplay between cellular structural organization, metabolic regulation, and neuroinflammatory processes in neurodegeneration.
Figures are computed from collected data and may differ slightly.
Previous studies that have investigated the potential of in vivo abnormal α-synuclein deposits as a pathological biomarker for PD included few participants and reported different diagnostic accuracies. Here, we aimed to confirm the diagnostic value of in vivo α-synuclein deposits in PD through a systematic review and meta-analysis, with special emphasis on determining the tissue most suitable for examination and assessing whether anti-native α-synuclein or anti-phosphorylated α-synuclein antibod
京都大学
This study provides Class II evidence that the CSF proteome contains clinically important information regarding the development and progression of Parkinson disease that can be deciphered by a combination of high-throughput proteomics and machine learning.
Epithelial/endothelial cells adhere to each other via cell-cell junctions including tight junctions (TJs) and adherens junctions (AJs). TJs and AJs are spatiotemporally and functionally integrated, and are thus often collectively defined as apical junctional complexes (AJCs), regulating a number of spatiotemporal events including paracellular barrier, selective permeability, apicobasal cell polarity, mechano-sensing, intracellular signaling cascades, and epithelial morphogenesis. Over the past 1
Liquid-liquid phase separation (LLPS) is involved in various dynamic biological phenomena. In epithelial cells, dynamic regulation of junctional actin filaments tethered to the apical junctional complex (AJC) is critical for maintaining internal homeostasis against external perturbations; however, the role of LLPS in this process remains unknown. Here, after identifying a multifunctional actin nucleator, cordon bleu (Cobl), as an AJC-enriched microtubule-associated protein, we conducted comprehe
Neuroinflammatory changes in the brain, including infiltration of lymphocytes, particularly T cells, play a critical role in the pathogenesis of Parkinson's disease (PD).1, 2 Interestingly, in the peripheral blood of PD patients, a decrease in circulating lymphocyte counts occurs, mainly due to a decrease in T cells.1, 3 Furthermore, it has recently been reported that lower lymphocyte count might be causally related to the subsequent development of PD.4 Inspired by these observations, we aimed a
A 46-year-old man presented with a history of personality change and memory disturbance for 5 months. He gradually became difficult in doing a daily job. Brain MRI showed abnormal hyperintensity within bilateral mesial temporal lobes on T<sub>2</sub> weighted image. Therefore, viral and autoimmune limbic encephalitis was initially suspected. However, because treponemal and non-treponemal specific antibodies were positive in serum and cerebrospinal fluid (CSF), the diagnosis of neurosyphilis was
Our study delineated the ultrasonographic features of IgM/anti-MAG neuropathy in the Japanese population and observed similar characteristics to those of t-CIDP, with subtle differences. Further studies comparing results from various populations are required to optimize the use of nerve ultrasound worldwide.
Abstract The proteome encodes for various information. By quantifying 4071 human proteins in the cerebrospinal fluid using high-throughput affinity proteomics, this study aimed to extract proteomic signatures associated with Parkinson’s disease using unbiased machine-learning and to examine their impact on Parkinson’s disease course. From the Parkinson’s Progression Markers Initiative, we first included 312 drug-naïve patients with Parkinson’s disease without GBA1 , LRRK2 , and SNCA mutations (n
We thank Dr. Grippe et al.1 for the constructive comment on our article. Along with highlighting important references,2,3 they reasonably urged caution in the interpretation of our results based on the inherent limitation of observational studies that “reverse causation” cannot be ruled out. These authors also note concern for the use of the Physical Activity Scale for the Elderly questionnaire to quantify regular physical activity and exercise habits. We fully agree with these points.
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