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Advertising Effectiveness through Sexual Appeal Model in Apparel Print Advertising: A Comparison Study between Chinese and Taiwanese Consumers
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天然酚酸改善高熱量飲食引起之混合型失智症大鼠學習與記憶損傷的評估及其機制探討
No full text[[abstract]]Type 2 diabetes mellitus (T2 DM) is characterized by insulin resistance. The high dietary energy (calorie) intake is among the major causes of T2 DM. Alzheimer's disease (AD) is the most common type of progressive dementia. Recent epidemiological studies linked the relation between insulin resistance and AD, and proposed the hypothesis of insulin involvement in the modulation of AD-related proteins such as β-amyloid. Insulin resistance in brain tissue promotes the formation of these proteins and aggravates the learning and memory impairments. In diagnosis, T2 DM combined with AD is recognized as a form of “mixed dementia” (Kulji? and Salkovi?-Petri?i?, 2011). The applicant is currently conducting an NSC project (NSC 100-2313-B-003-001), and has proved the effectiveness of naturally occurred phenolic acids in reducing blood sugar level in T2 DM rats. Reported studies pertaining to the relation of naturally occurred phenolic acids to brain insulin resistance induced dementia are very limited, although significant academic and practical values are expectable. The insulin-resistant Neuro 2a (N2A) mouse neuroblastoma cell model has been established by our laboratory. The applicant has also obtained preliminary data to show the enhancement of glucose uptake from certain naturally occurred phenolic acids, for example caffeic acid and cinnamic acid in insulin resistant neuron cells, indicating their alleviative potential in brain insulin resistance induced dementia. The behavior tests for dementia animal model have already been established in our laboratory. These key techniques render this research proposal to be implemented successfully once it is approved. The aim of this project is to investigate the alleviative effect of naturally occurred phenolic acids on learning and memory impairments in high-calorie diet induced mixed dementia rats. In this three-year project, (1) first, insulin-resistant N2A cells will be used in the screening for phenolic acids that promote glucose uptake. High-calorie diet induced mixed dementia animal experiments will be performed and Morris water maze task will be conducted to confirm their effects. The brain histology and some specific brain biochemical values will also be analyzed. (2) Second, the protein expressions of neuron carbohydrate metabolic enzymes, neuron insulin signaling, and inflammatory factors in brain tissues of rats will be determined to elucidate the mechanism of phenolic acids on improving brain insulin resistance in high-calorie diet induced mixed dementia rats. (3) Finally, protein expressions of neuronal signaling and neuronal plasticity in cortical neurons will be analyzed, and proteomics studies will be performed. A possible mechanism for phenolic acid to improve the brain neuronal signaling and neural plasticity in high-calorie diet induced mixed dementia will be proposed. The completion of the project shall be helpful for understanding on the alleviative effect of phenolic acids in high-calorie induced mixed dementia. In addition, it is also helpful for the understanding of the etiology of brain insulin resistance induced dementia and the mechanism for phenolic acids in relieving the symptom.
