Kyushu University Academic Staff Educational and Research Activities Database
List of Reports
Ryo Yamasaki Last modified date:2022.06.13

Associate Professor / Neurology / Neurological Institute / Faculty of Medical Sciences

1. Intractable facial pain in advanced Parkinson's disease alleviated by subthalamic stimulation : A case report.
2. Intraoperative hemorrhagic complication during multi-track microelectrode recording in stereotactic functional neurosurgery.
3. Non-motor effect of chronic subthalamic stimulation and dopamine replacement therapy for advanced Parkinson's disease.
4. Jun-Ichi Kira, Ryo Yamasaki, Katsuhisa Masaki, Neuro2013, Clinical and Experimental Neuroimmunology, 10.1111/cen3.12042, Vol.4, No.2, pp.243-245, 2013.08.
5. Jun-Ichi Kira, Ryo Yamasaki, Hidenori Ogata, Anti-neurofascin autoantibody and demyelination., Neurochemistry international, 10.1016/j.neuint.2018.12.011, Vol.130, p.104360, 2019.11, Demyelination diseases involving the central and peripheral nervous systems are etiologically heterogeneous with both cell-mediated and humoral immunities playing pathogenic roles. Recently, autoantibodies against nodal and paranodal proteins, such as neurofascin186 (NF186), neurofascin155 (NF155), contactin-1 (CNTN1), contactin-associated protein 1 (CASPR1) and gliomedin, have been discovered in not only chronic demyelinating conditions, such as multiple sclerosis (MS) and chronic inflammatory demyelinating polyradiculoneuropathy, but also in acute demyelinating conditions, such as Guillain-Barré syndrome. Only a minority of these patients harbor anti-nodal/paranodal protein antibodies; however, these autoantibodies, especially IgG4 subclass autoantibodies to paranodal proteins, are associated with unique features and these conditions are collectively termed nodopathy or paranodopathy. Establishing a concept of IgG4-related nodopathy/paranodopathy contributes to diagnosis and treatment strategy because IgG4 autoantibody-related neurological diseases are often refractory to conventional immunotherapies. IgG4 does not fix complements, or internalize the target antigens, because IgG4 exists in a monovalent bispecific form in vivo. IgG4 autoantibodies can bock protein-protein interaction. Thus, the primary role of IgG4 anti-paranodal protein antibodies may be blockade of interactions between NF155 and CNTN1/CASPR1, leading to conduction failure, which is consistent with the sural nerve pathology presenting paranodal terminal loop detachment from axons with intact internodes in the absence of inflammation. However, it still remains to be elucidated how these autoantibodies belonging to the same IgG4 subclass can cause each IgG4 autoantibody-specific manifestation. Another important issue is to clarify the mechanism by which IgG4 antibodies to nodal/paranodal proteins emerge. IgG4 antibodies develop on chronic antigenic stimulation and can block antibodies that alleviate allergic inflammation by interfering with the binding of allergen-specific IgE to allergens. Thus, environmental antigens cross-reacting with nodal and paranodal proteins may warrant future study..
6. Autoantibody in chronic inflammatory neuropathies.
7. Ryo Yamasaki, Anti-neurofascin antibody in combined central and peripheral demyelination., Clinical and Experimental Neuroimmunology, 2013.12, Neurofascin (NF), one of the cell adhesion molecules expressed in both central nervous system (CNS) and peripheral nervous system (PNS), plays important roles in developing and maintaining the neural structures. There are several subtypes of NF resulted from the post-translational modifications; NF155, 166, 180 and 186. Among them, NF155 and NF186 are expressed in the mature CNS/PNS. NF155 is present on the oligodendroglial cell surface in CNS and Schwann cell surface in PNS at the paranode, which tightly connects with contactin and caspr on the axonal surface of paranode and works as a stabilizer of the node of Ranvier. NF186 exists on the axonal surface at the node of Ranvier. NF186 is associated with voltage gated Na channels (Nav) while both NF186 and Nav are anchored by ankyrin G. NF186 contributes to clustering of Nav at the node.
Combined central and peripheral demyelination (CCPD) is an inflammatory demyelinating disorder affecting both the CNS and PNS tissues. In this condition, distinct mechanisms from multiple sclerosis (MS) or chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are hypothesized, based on the distinctive clinical and laboratory findings. We detected anti-NF155 antibody by cell-based assay, enzyme-linked immunosorbent assay and western blot in both sera and cerebrospinal fluids of CCPD patients at high frequencies while not in patients with other neurological disease or healthy controls. I hereby summarize basic aspects and clinical significance of NFs as indispensable regulators and autoimmune target molecules.