Data on amyloid precursor protein accumulation, spontaneous physical activity, and motor learning after traumatic brain injury in the triple-transgenic mouse model of Alzheimer׳s disease

Yasushi Kishimoto; Hajime Shishido; Mayumi Sawanishi; Yasunori Toyota; Masaki Ueno; Takashi Kubota; Yutaka Kirino; Takashi Tamiya; Nobuyuki Kawai

doi:10.1016/j.dib.2016.08.041

Data on amyloid precursor protein accumulation, spontaneous physical activity, and motor learning after traumatic brain injury in the triple-transgenic mouse model of Alzheimer׳s disease

Data Brief. 2016 Aug 26:9:62-7. doi: 10.1016/j.dib.2016.08.041. eCollection 2016 Dec.

Authors

Yasushi Kishimoto¹, Hajime Shishido², Mayumi Sawanishi¹, Yasunori Toyota², Masaki Ueno³, Takashi Kubota¹, Yutaka Kirino¹, Takashi Tamiya², Nobuyuki Kawai⁴

Affiliations

¹ Laboratory of Neurobiophysics, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Japan.
² Department of Neurological Surgery, Faculty of Medicine, Kagawa University, Japan.
³ Department of Inflammation Pathology, Faculty of Medicine, Kagawa University, Japan.
⁴ Department of Neurological Surgery, Faculty of Medicine, Kagawa University, Japan; Department of Neurological Surgery Kagawa General Rehabilitation Hospital, Japan.

Abstract

This data article contains supporting information regarding the research article entitled "Traumatic brain injury accelerates amyloid-β deposition and impairs spatial learning in the triple-transgenic mouse model of Alzheimer׳s disease" (H. Shishido, Y. Kishimoto, N. Kawai, Y. Toyota, M. Ueno, T. Kubota, Y. Kirino, T. Tamiya, 2016) [1]. Triple-transgenic (3×Tg)-Alzheimer׳s disease (AD) model mice exhibited significantly poorer spatial learning than sham-treated 3×Tg-AD mice 28 days after traumatic brain injury (TBI). Correspondingly, amyloid-β (Aβ) deposition within the hippocampus was significantly greater in 3×Tg-AD mice 28 days after TBI. However, data regarding the short-term and long-term influences of TBI on amyloid precursor protein (APP) accumulation in AD model mice remain limited. Furthermore, there is little data showing whether physical activity and motor learning are affected by TBI in AD model mice. Here, we provide immunocytochemistry data confirming that TBI induces significant increases in APP accumulation in 3×Tg-AD mice at both 7 days and 28 days after TBI. Furthermore, 3×Tg-AD model mice exhibit a reduced ability to acquire conditioned responses (CRs) during delay eyeblink conditioning compared to sham-treated 3×Tg-AD model mice 28 days after TBI. However, physical activity and motor performance are not significantly changed in TBI-treated 3×Tg-AD model mice.

Keywords: AD, Alzheimer׳s disease; ANOVA, analysis of variance; APP, amyloid precursor protein; Amyloid precursor protein; CR, conditioned response; CS, conditioned stimulus; Eyeblink conditioning; Rotarod test; Spontaneous physical activity; TBI, traumatic brain injury; Traumatic brain injury; US, unconditioned stimulus.