Learning and Memory Performance of Alzheimer Disease Mouse Model with Mutant Human Tau Protein
Description: rTg4510 mice constitutively express mutant human tau protein until transgene expression is inactivated by administration of the doxycycline (DOX). In 6-month-old (young) rTg4510 mice, the hippocampus dependent learning abilities including spatial memory, object recognition memory, and trace eyeblink conditioning were impaired. These impairments were reduced by pre-treatment with DOX for 2 months. In parallel, the expression of NFTs decreased in DOX-treated group. 10-month-old (aged) rTg4510 mice showed severe recognition impairment and increased levels of NFTs. Treatment with DOX could not ameliorate the tau pathology in aged rTg4510 mice as well as DOX-untreated group. Since the amount of autophagy markers decreased along with the amelioration of tau pathology, clearance mechanisms of NFTs via autophagy have kept normal functions in 4- to 6-month-old mice while, in 10-month-old mice, clearance system may reach a saturation level.
Amount: ¥4,810,000
Funding type: research
Funder scheme: Grant-in-Aid for Scientific Research (C)
Start date: 2016-04-01
End date: 2020-03-31
Investigator: Yutaka Kirino
Institution: Tokushima Bunri University
Funded outputs count: 4
Funder award ID: 16K08215
OpenAlex ID: G1961687491