A boy with autism spectrum disorder with antibodies to the NMDA-type glutamate receptor: nine-year follow-up, changes in cognitive function

Tomoko Takeuchi; Takashi Enokizono; Mai Tanaka; Takayoshi Jin; Yukitoshi Takahashi; Hidetoshi Takada

doi:10.1080/09297049.2025.2495232

A boy with autism spectrum disorder with antibodies to the NMDA-type glutamate receptor: nine-year follow-up, changes in cognitive function

Child Neuropsychol. 2025 Apr 22:1-8. doi: 10.1080/09297049.2025.2495232. Online ahead of print.

Authors

Tomoko Takeuchi¹, Takashi Enokizono^{2

3}, Mai Tanaka², Takayoshi Jin⁴, Yukitoshi Takahashi⁵, Hidetoshi Takada^{2

3}

Affiliations

¹ Department of Clinical Psychology, University of Tsukuba Hospital, Ibaraki, Japan.
² Department of Pediatrics, University of Tsukuba Hospital, Ibaraki, Japan.
³ Department of Child Health, Institute of Medicine, University of Tsukuba, Ibaraki, Japan.
⁴ Department of Medical Services, Ibaraki Prefectural Medical Center of Psychiatry, Ibaraki, Japan.
⁵ National Epilepsy Center, NHO Shizuoka Institute of Epilepsy and Neurological Disorders, Shizuoka, Japan.

PMID: 40260642
DOI: 10.1080/09297049.2025.2495232

Abstract

Herein, we report a 12-year-old boy with autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) who showed a cognitive decline at age 7 and tested positive for cerebrospinal fluid (CSF) N-methyl-D-aspartate (NMDA)-type glutamate receptor (GluR) antibodies using an enzyme-linked immunosorbent assay (ELISA). His cognitive function developed between ages 3 and 5, reaching a total domain developmental quotient (DQ) of 61 on the revised Kyoto Scale of Psychological Development 2001. Despite multiple treatments, his total domain DQ declined to 21 at 10 years and 3 months of age and further to 16 at 12 years and 0 month. The child regressed in cognitive function, losing previously acquired knowledge and skills, resulting in an unbalanced profile. Previously recorded strengths, weaknesses, and preferences were no longer evident. The anti-NMDA-type GluR antibodies might hinder the regaining of cognitive functions once lost and the reconstruction of developmental characteristics in patients with ASD/ADHD. Patients with ASD and ADHD who test positive for NMDA-type GluR antibodies (ELISA) may not follow a typical clinical course.

Keywords: Anti-NMDA-type glutamate receptor antibodies; attention deficit hyperactivity disorder; autism spectrum disorder; cognitive function; enzyme-linked immunosorbent assay.