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Page 18 of 24 Neuroimmunol Neuroinflammation 2019;6:15 I http://dx.doi.org/10.20517/2347-8659.2019.019

improvement and clinical recovery. The results were analyzed using the reliable change index. The results
reveal that the patient improved her intellectual abilities, attention, and visuospatial abilities. They also
improved the skills of abstraction and memory. In the literature, it is related that the neuropsychological
intervention stimulates the activation of alternative or inactive neural networks that begin to have a greater
implication in the affected cognitive processes. These findings demonstrate that neuropsychological
intervention is an effective therapeutic strategy for patients with congenital brain damage.

25. Caspr2/CNTNAP2 (or cadm1) forms a complex with GPR37 and Mupp1 but not with
autism-related mutated ones

1
1
1
Eriko Jimbo-Fujita , Takanori Yamagata , Hidetosi Takahasi , Yukiko Hayashi , Mariko Yoshida
1
Momoi , Takashi Momoi 2
2
1 Department of Pediatrics, Jichi meedical University, Japan
2 Department of Pathophysiology, Tokyo medical University, Japan

Autism spectrum disorder (ASD) is one of the developmental brain disorders. Mutations in the synaptic
components including NLGN, Nrx, Cadm1, Caspr2/CNTNAP2 (Contactin-associated protein 2), and
GPR37 (G-protein-coupled receptor 37) have been found in ASD patients. Caspr2 and Cadm1 have a PDZ
binding domain at C-terminal region and form a complex with receptors via interaction with Multiple PDZ
domain protein 1 (Mupp1). However, little is known about the impaired Caspr2 (Cadm1)-Mupp1-receptor
complex related to the pathogenesis of ASD. Recently, we found mutations (R558Q and Del312F) of GPR37
gene in the ASD patients. Caspr2 (Cadm1) and GPR37 mainly interacted with PDZ3 and PDZ11 domains
of Mupp1 via their C-terminal PDZ binding domains, respectively, while the ASD-associated mutated
GPR37 (R558Q) more weakly interacted with Mupp1 and was much less transported to the cell surface by
Mupp1. In the present study, we found two missense mutations in Mupp1 gene of the ASD patients and
investigated the density and morphology of PSD95-positive dendritic spines and protrusions in cultured
hippocampal neurons overexpressing the mutated Mupp1. Compared to the Mupp1, mutated Mupp1
significantly reduced the density of PSD95-positive dendritic spines and decreased the width of dendritic
spines. Thus, ASD-related Mupp1 missense mutations influence the dendritic spine morphogenesis, causing
the pathogenesis of ASD. The impaired Caspr2 (Cadm1)-Mupp1-receptor complex including Gpr37 or
serotine receptors may be related to the pathogenesis of ASD.

26. The prognostic factors affecting the occurrence of subsequent unprovoked seizure in

patients who present with febrile seizure after 6 years of age

Seung Hyo Kim

Department of Pediatrics, Jeju National University College of Medicine, Jeju, Korea

Aim: Few reports have described the prognostic factors affecting the occurrence of subsequent unprovoked
seizure in patients who present with febrile seizure (FS) after six years of age. We investigated the
prognostic factors affecting the development of unprovoked seizures after FS among patients from Jeju
Island.