Neuronal TDP-43 regulates myelin formation via neurexin 1 mRNA stabilization

J Jiayi Li Y Yohei Iguchi (Department of Neurology, Nagoya University Graduate School of Medicine) K Kenji Yoshida (Department of Anatomy and Molecular Cell Biology, Nagoya University Graduate School of Medicine) D Daisuke Kato K Kunihiko Araki (Department of Neurology, Nagoya University Graduate School of Medicine) K Kenta Kobayashi (Section of Viral Vector Development, National Institute for Physiological Sciences) S Satoshi Yokoi (Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine) R Rei Yoshimoto (Department of Applied Biological Sciences, Faculty of Agriculture, Setsunan University) M Madoka Iida (Department of Neurology, Nagoya University Graduate School of Medicine) Y Yoshinobu Amakusa (Department of Neurology, Nagoya University Graduate School of Medicine) Y Yu Kawakami (Department of Neurology, Nagoya University Graduate School of Medicine) T Takashi Yoshimura (Department of Neurology, Nagoya University Graduate School of Medicine) R Ryo Chikuchi (Department of Neurology, Nagoya University Graduate School of Medicine) K Koyo Tsujikawa (Department of Neurology, Nagoya University Graduate School of Medicine) Y Yuichi Riku (Department of Neurology, Nagoya University Graduate School of Medicine) Y Yasushi Iwasaki (Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University) Y Yohei Okada (Department of Neural iPSC Research, Institute for Medical Science of Aging, Aichi Medical University) N Nobuhiko Ohno (Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University) H Hiroaki Wake M Masahisa Katsuno (Department of Neurology, Nagoya University Graduate School of Medicine)

Abstract

Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) develop as spatial pathologies in which neurons and glial cells are interconnected. TAR DNA-binding protein 43 (TDP-43) is a major pathological protein that is inextricably associated with ALS and FTLD. In this study, we investigated the roles of neuronal TDP-43 in neuron–oligodendrocyte interactions using neuron-specific TDP-43 knockout (TDP-43cKO) mice. TDP-43 depletion in neurons induced hypomyelination, which was confirmed by immunohistochemistry and ultrastructural analysis. In addition, conduction disturbance was revealed by electrophysiological analysis. The hypomyelination of TDP-43cKO mouse was restored by cytoplasmic TDP-43 supplementation in neurons. Neuron-specific transcriptome analysis revealed that neurexin 1 (NRXN1) is the regulatory target of TDP-43, which promotes myelin formation. The hypomyelination of TDP-43cKO mice was also restored by NRXN1b supplementation in neurons. We further confirmed that TDP-43 stabilizes Nrxn1 mRNA by binding to the Nrxn1 3’untranslated region (3’UTR). Although TDP-43cKO exhibited impaired recognition memory, the supplementation of NRXN1 in the hippocampus recovered the memory disturbances. In conclusion, this study demonstrates the neuron–oligodendrocyte interaction mediated by neuronal TDP-43 via NRXN1 mRNA stabilization. These findings shed light on neuron–oligodendrocyte interaction in the disease mechanisms of ALS/FTLD.

Article Details

Volume / Issue Vol. 123, Issue 9
Published March 03, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (20)

J

Jiayi Li

Y

Yohei Iguchi

Department of Neurology, Nagoya University Graduate School of Medicine

K

Kenji Yoshida

Department of Anatomy and Molecular Cell Biology, Nagoya University Graduate School of Medicine

D

Daisuke Kato

K

Kunihiko Araki

Department of Neurology, Nagoya University Graduate School of Medicine

K

Kenta Kobayashi

Section of Viral Vector Development, National Institute for Physiological Sciences

S

Satoshi Yokoi

Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine

R

Rei Yoshimoto

Department of Applied Biological Sciences, Faculty of Agriculture, Setsunan University

M

Madoka Iida

Department of Neurology, Nagoya University Graduate School of Medicine

Y

Yoshinobu Amakusa

Department of Neurology, Nagoya University Graduate School of Medicine

Y

Yu Kawakami

Department of Neurology, Nagoya University Graduate School of Medicine

T

Takashi Yoshimura

Department of Neurology, Nagoya University Graduate School of Medicine

R

Ryo Chikuchi

Department of Neurology, Nagoya University Graduate School of Medicine

K

Koyo Tsujikawa

Department of Neurology, Nagoya University Graduate School of Medicine

Y

Yuichi Riku

Department of Neurology, Nagoya University Graduate School of Medicine

Y

Yasushi Iwasaki

Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University

Y

Yohei Okada

Department of Neural iPSC Research, Institute for Medical Science of Aging, Aichi Medical University

N

Nobuhiko Ohno

Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University

H

Hiroaki Wake

M

Masahisa Katsuno

Department of Neurology, Nagoya University Graduate School of Medicine