Acid-Sensing Ion Channel 1 Deficiency Aggravates Cuprizone-Induced Demyelination, Axonal Damage and Microgliosis in Mice
- 1University of Bonn, University Hospital Bonn, Anatomy and Cell Biology, 53127 Bonn, Germany
- 2Department of Biophysics, Faculty of Medicine, Süleyman Demirel University, Isparta 32260, Türkiye
- 3Institute of Physiology, RWTH Aachen University, 52074 Aachen, Germany
Abstract
White matter degeneration in multiple sclerosis (MS) is characterized by oligodendrocyte dysfunction and subsequent demyelination. To determine whether acid-sensing ion channel subtype 1 (ASIC1) contributes to oligodendrocyte-associated pathology under non-autoimmune conditions, the cuprizone model was used in wild-type (WT) and ASIC1-deficient (KO) mice. Axonal degeneration, microgliosis (IBA1), demyelination, and oligodendrocyte abundance were assessed in the medial Corpus Callosum. Cuprizone increased IBA1 positivity, axonal damage, and demyelination, and these effects appeared more pronounced in ASIC1 KO animals than in WT animals. ASIC1 deficiency was associated with increased APP+ axonal spheroid formation and reduced myelination scores. However, oligodendrocyte marker analyses did not indicate an additional reduction in oligodendrocyte survival after 3 weeks. Overall, these data support a role of ASIC1 in preserving myelin integrity, consistent with myelin maintenance rather than direct regulation of oligodendrocyte survival.
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BibTeX
@article{oz2026acidsensing,
title = {{Acid-Sensing Ion Channel 1 Deficiency Aggravates Cuprizone-Induced Demyelination, Axonal Damage and Microgliosis in Mice}},
author = {Ahmi Öz and Dominik Wiemuth and Stefan Gründer and Tim Clarner and Natalie Tillmann},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219758},
url = {https://www.mdpi.com/1422-0067/27/21/9758},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Acid-Sensing Ion Channel 1 Deficiency Aggravates Cuprizone-Induced Demyelination, Axonal Damage and Microgliosis in Mice
AU - Ahmi Öz
AU - Dominik Wiemuth
AU - Stefan Gründer
AU - Tim Clarner
AU - Natalie Tillmann
PY - 2026
DA - 2026/10/30
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219758
UR - https://www.mdpi.com/1422-0067/27/21/9758
AB - White matter degeneration in multiple sclerosis (MS) is characterized by oligodendrocyte dysfunction and subsequent demyelination. To determine whether acid-sensing ion channel subtype 1 (ASIC1) contributes to oligodendrocyte-associated pathology under non-autoimmune conditions, the cuprizone model was used in wild-type (WT) and ASIC1-deficient (KO) mice. Axonal degeneration, microgliosis (IBA1), demyelination, and oligodendrocyte abundance were assessed in the medial Corpus Callosum. Cuprizone increased IBA1 positivity, axonal damage, and demyelination, and these effects appeared more pronounced in ASIC1 KO animals than in WT animals. ASIC1 deficiency was associated with increased APP+ axonal spheroid formation and reduced myelination scores. However, oligodendrocyte marker analyses did not indicate an additional reduction in oligodendrocyte survival after 3 weeks. Overall, these data support a role of ASIC1 in preserving myelin integrity, consistent with myelin maintenance rather than direct regulation of oligodendrocyte survival.
SN - 1422-0067
ER -