Abstract
Obesity-related metabolic disorders can affect not only systemic health but also brain function. Recent studies have elucidated that amyloid beta deposition cannot satisfactorily explain the development of Alzheimer's disease (AD) and that dysregulation of glucose metabolism is a critical factor for the sporadic onset of non-genetic AD. Identifying the pathophysiology of AD due to changes in brain metabolism is crucial; however, it is limited in measuring changes in brain cognitive function due to metabolic changes in animal models. The touchscreen-based automated battery system, which is more accurate and less invasive than conventional behavioral test tools, is used to assess the cognition of mice with dysregulated metabolism. This system was introduced in humans to evaluate cognitive function and was recently back-translated in monkeys and rodents. We used outbred ICR mice fed on highfat diet (HFD) and performed the paired associates learning (PAL) test to detect their visual memory and new learning ability loss as well as to assess memory impairment. The behavioral performance of the HFD mice was weaker than that of normal mice in the training but was not significantly associated with motivation. In the PAL test, the average number of trials completed and proportion of correct touches was significantly lower in HFD mice than in normal diet-fed mice. Our results reveal that HFD-induced metabolic dysregulation has detrimental effects on operant learning according to the percentage of correct responses in PAL. These findings establish that HFD-induced metabolic stress may have an effect in accelerating AD-like pathogenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 277-286 |
| Number of pages | 10 |
| Journal | Experimental Neurobiology |
| Volume | 27 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 2018 Aug 1 |
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All Science Journal Classification (ASJC) codes
- Clinical Neurology
- Cellular and Molecular Neuroscience
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Assessment of cognitive impairment in a mouse model of high-fat diet-induced metabolic stress with touchscreen-based automated battery system. / Lee, Saeram; Kim, Jong Youl; Kim, Eosu; Seo, KyoungYul; Kang, Youn Jae; Kim, Jae Young; Kim, Chul Hoon; Song, Ho Taek; Saksida, Lisa M.; Lee, Jongeun.
In: Experimental Neurobiology, Vol. 27, No. 4, 01.08.2018, p. 277-286.Research output: Contribution to journal › Article
TY - JOUR
T1 - Assessment of cognitive impairment in a mouse model of high-fat diet-induced metabolic stress with touchscreen-based automated battery system
AU - Lee, Saeram
AU - Kim, Jong Youl
AU - Kim, Eosu
AU - Seo, KyoungYul
AU - Kang, Youn Jae
AU - Kim, Jae Young
AU - Kim, Chul Hoon
AU - Song, Ho Taek
AU - Saksida, Lisa M.
AU - Lee, Jongeun
PY - 2018/8/1
Y1 - 2018/8/1
N2 - Obesity-related metabolic disorders can affect not only systemic health but also brain function. Recent studies have elucidated that amyloid beta deposition cannot satisfactorily explain the development of Alzheimer's disease (AD) and that dysregulation of glucose metabolism is a critical factor for the sporadic onset of non-genetic AD. Identifying the pathophysiology of AD due to changes in brain metabolism is crucial; however, it is limited in measuring changes in brain cognitive function due to metabolic changes in animal models. The touchscreen-based automated battery system, which is more accurate and less invasive than conventional behavioral test tools, is used to assess the cognition of mice with dysregulated metabolism. This system was introduced in humans to evaluate cognitive function and was recently back-translated in monkeys and rodents. We used outbred ICR mice fed on highfat diet (HFD) and performed the paired associates learning (PAL) test to detect their visual memory and new learning ability loss as well as to assess memory impairment. The behavioral performance of the HFD mice was weaker than that of normal mice in the training but was not significantly associated with motivation. In the PAL test, the average number of trials completed and proportion of correct touches was significantly lower in HFD mice than in normal diet-fed mice. Our results reveal that HFD-induced metabolic dysregulation has detrimental effects on operant learning according to the percentage of correct responses in PAL. These findings establish that HFD-induced metabolic stress may have an effect in accelerating AD-like pathogenesis.
AB - Obesity-related metabolic disorders can affect not only systemic health but also brain function. Recent studies have elucidated that amyloid beta deposition cannot satisfactorily explain the development of Alzheimer's disease (AD) and that dysregulation of glucose metabolism is a critical factor for the sporadic onset of non-genetic AD. Identifying the pathophysiology of AD due to changes in brain metabolism is crucial; however, it is limited in measuring changes in brain cognitive function due to metabolic changes in animal models. The touchscreen-based automated battery system, which is more accurate and less invasive than conventional behavioral test tools, is used to assess the cognition of mice with dysregulated metabolism. This system was introduced in humans to evaluate cognitive function and was recently back-translated in monkeys and rodents. We used outbred ICR mice fed on highfat diet (HFD) and performed the paired associates learning (PAL) test to detect their visual memory and new learning ability loss as well as to assess memory impairment. The behavioral performance of the HFD mice was weaker than that of normal mice in the training but was not significantly associated with motivation. In the PAL test, the average number of trials completed and proportion of correct touches was significantly lower in HFD mice than in normal diet-fed mice. Our results reveal that HFD-induced metabolic dysregulation has detrimental effects on operant learning according to the percentage of correct responses in PAL. These findings establish that HFD-induced metabolic stress may have an effect in accelerating AD-like pathogenesis.
UR - http://www.scopus.com/inward/record.url?scp=85053307930&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85053307930&partnerID=8YFLogxK
U2 - 10.5607/en.2018.27.4.277
DO - 10.5607/en.2018.27.4.277
M3 - Article
AN - SCOPUS:85053307930
VL - 27
SP - 277
EP - 286
JO - Experimental Neurobiology
JF - Experimental Neurobiology
SN - 1226-2560
IS - 4
ER -