Publikasi Scopus 2024 per tanggal 29 Februari 2024 (130 artikel)

Riset dan Pengabdian Masyarakat Do Research Sosial Service and Innovation

Publikasi Scopus 2024 per tanggal 29 Februari 2024 (130 artikel)

Authors

Murakami T.; Abe M.; Tiksnadi A.; Nemoto A.; Futamura M.; Yamakuni R.; Kubo H.; Kobayashi N.; Ito H.; Hanajima R.; Hashimoto Y.; Ugawa Y.

Full Names

Murakami, Takenobu (8338216800); Abe, Mitsunari (7404123222); Tiksnadi, Amanda (57204616263); Nemoto, Ayaka (57191277352); Futamura, Miyako (56513608000); Yamakuni, Ryo (57218920456); Kubo, Hitoshi (7402808606); Kobayashi, Naoto (58812488900); Ito, Hiroshi (7407939846); Hanajima, Ritsuko (7004551024); Hashimoto, Yasuhiro (56397195500); Ugawa, Yoshikazu (7005460744)

Author S Id

8338216800; 7404123222; 57204616263; 57191277352; 56513608000; 57218920456; 7402808606; 58812488900; 7407939846; 7004551024; 56397195500; 7005460744

Title

Abnormal motor cortical plasticity as a useful neurophysiological biomarker for Alzheimer's disease pathology

Year

2024

Source Title

Clinical Neurophysiology

Volume

158

Issue

Art No

Page Start

170

Page End

179

Page Count

Cited By

Link

https://www.scopus.com/inward/record.uri?eid=2-s2.0-85182348160&doi=10.1016%2fj.clinph.2023.12.131&partnerID=40&md5=6f67aee1633f26ea838909c3d364d401

Affiliations

Department of Neurology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University, Nishimachi 36-1, Yonago, 683-8504, Japan; Center for Neurological Disorders, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Department of Neurology, Cipto Mangunkusumo Hospital, Faculty of Medicine, Universitas Indonesia, Salemba Raya No. 6, Jakarta, 10430, Indonesia; Advanced Clinical Research Center, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Rehabilitation Center, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Department of Radiology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Department of Radiological Sciences, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Azuma Street Clinic, Sakaemachi 1-28, Fukushima, 960-8031, Japan; Department of Biochemistry, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Department of Human Neurophysiology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan

Authors With Affiliations

Murakami T., Department of Neurology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan, Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University, Nishimachi 36-1, Yonago, 683-8504, Japan; Abe M., Center for Neurological Disorders, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Tiksnadi A., Department of Neurology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan, Department of Neurology, Cipto Mangunkusumo Hospital, Faculty of Medicine, Universitas Indonesia, Salemba Raya No. 6, Jakarta, 10430, Indonesia; Nemoto A., Advanced Clinical Research Center, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Futamura M., Rehabilitation Center, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Yamakuni R., Department of Radiology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Kubo H., Advanced Clinical Research Center, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan, Department of Radiological Sciences, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Kobayashi N., Azuma Street Clinic, Sakaemachi 1-28, Fukushima, 960-8031, Japan; Ito H., Advanced Clinical Research Center, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan, Department of Radiology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Hanajima R., Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University, Nishimachi 36-1, Yonago, 683-8504, Japan; Hashimoto Y., Department of Biochemistry, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan; Ugawa Y., Department of Neurology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan, Department of Human Neurophysiology, Faculty of Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima, 960-1295, Japan

Abstract

Objective: Amyloid-beta (Aβ) and tau accumulations impair long-term potentiation (LTP) induction in animal hippocampi. We investigated relationships between motor-cortical plasticity and biomarkers for Alzheimer's disease (AD) diagnosis in subjects with cognitive decline. Methods: Twenty-six consecutive subjects who complained of memory problems participated in this study. We applied transcranial quadripuse stimulation with an interstimulus interval of 5 ms (QPS5) to induce LTP-like plasticity. Motor-evoked potentials were recorded from the right first-dorsal interosseous muscle before and after QPS5. Cognitive functions, Aβ42 and tau levels in the cerebrospinal fluid (CSF) were measured. Amyloid positron-emission tomography (PET) with 11C-Pittsburg compound-B was also conducted. We studied correlations of QPS5-induced plasticity with cognitive functions or AD-related biomarkers. Results: QPS5-induced LTP-like plasticity positively correlated with cognitive scores. The degree of LTP-like plasticity negatively correlated with levels of CSF-tau, and the amount of amyloid-PET accumulation at the precuneus, and correlated with the CSF-Aβ42 level positively. In the amyloid-PET positive subjects, non-responder rate of QPS5 was higher than the CSF-tau positive rate. Conclusions: Findings suggest that QPS5-induced LTP-like plasticity is a functional biomarker of AD. QPS5 could detect abnormality at earlier stages than CSF-tau in the amyloid-PET positive subjects. Significance: Assessing motor-cortical plasticity could be a useful neurophysiological biomarker for AD pathology. © 2024 International Federation of Clinical Neurophysiology

Author Keywords

Alzheimer's disease; Amyloid beta; Long-term potentiation; Quadripulse stimulation; Synaptic plasticity; Tau; Transcranial magnetic stimulation

Index Keywords

Alzheimer Disease; Amyloid beta-Peptides; Biomarkers; Cognitive Dysfunction; Humans; Long-Term Potentiation; Positron-Emission Tomography; tau Proteins; amyloid beta protein[1-42]; biological marker; tau protein; amyloid beta protein; biological marker; tau protein; aged; Alzheimer disease; Article; cerebrospinal fluid analysis; clinical article; cognition; controlled study; female; human; male; motor evoked potential; nerve cell plasticity; neurophysiology; positron emission tomography; stimulation; cerebrospinal fluid; cognitive defect; diagnostic imaging; long term potentiation; pathology; physiology

Funding Details

Ministry of Education, Culture, Sports, Science and Technology, MEXT, (15H01563, 15H05881, 16H05322, 17K09809, 19H01091, 20K07866, 22390181, 23H00495, 25293206)

Funding Text

This work was supported in part by a grant to T.M. from the Grant-in-Aid for Scientific Research project of the Ministry of Education, Culture, Sports, Science and Technology (Grant 15H01563 ), and grants to Y.U. (Grants 22390181 , 25293206 , 15H05881 , 16H05322 , 17K09809 , 19H01091 , 20K07866 , and 23H00495 ).

Publisher

Elsevier Ireland Ltd

Issn

13882457

Isbn

Pubmed Id

38219406

Document Type

Article

Sjr Best Quartile

Sjr

1212

Sjr Rank

3032