| Summary: | 碩士 === 國立陽明大學 === 腦科學研究所 === 106 === Background: Alzheimer's disease (AD) is the most common form of dementia, accounting for approximately 60% of cases. In addition to memory lost, changes in pain sensitivity are found in a substantial proportion of AD patients. However, the association between the pain sensation deficit and AD is still unclear.
Aims and Hypotheses: We hypothesize that the pathological change of AD might affect the expression of N-methyl-D-aspartate receptor (NMDAR) NR2B subunit in hippocampus contributing to abnormal nociceptive processing.
Materials and Methods: To examine the pain sensitivity, von Frey filaments, capsaicin, tail flick and acetone tests were applied to assess the nociceptive response between wild type (WT) and AD mouse model at 6, 9 and 12 month of age. Novel object recognition were applied to evaluate memory impairments. In addition, western blot and qPCR would be assessed to quantify the expression of NMDAR NR2B subunit to figure out the correlation between nociception alteration and memory decline.
Results: AD mouse model had lower pain sensitivity to mechanical and thermal stimulation at different ages compared to WT groups. Meanwhile, the decreased amount of synaptic NR2B subunit and nNOS level might be responsible for the sensation alteration.
Conclusions: This study might clarify the mechanism for pain sensitivity alteration in AD mouse model and would improve the quality of daily care for AD patient.
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