Deficiency of base excision repair enzyme, OGG1 or MUTYH alters activation status of microglia, amyloid-beta burden, and behavior pattern in <I>App<SUP>NL-G-F</SUP></I> knock-in mouse model of Alzheimerʼs disease

Yuri Mizuno; Abolhassani Nona; Mazzei Guianfranco; Takashi Saito; Takaomi C. Saido; Yusaku  Nakabeppu

[4P-0471] Deficiency of base excision repair enzyme, OGG1 or MUTYH alters activation status of microglia, amyloid-beta burden, and behavior pattern in App^NL-G-F knock-in mouse model of Alzheimerʼs disease

〇Yuri Mizuno¹, Abolhassani Nona¹, Mazzei Guianfranco¹, Takashi Saito^2,3, Takaomi C. Saido³, Yusaku Nakabeppu¹ (1.Div. Neurofunctional Genomics, Med. Inst. Bioreg., Kyushu Univ., 2. Dept. Neurocognitive Sci., Grad. Sch. Med. Sci., Nagoya City Univ. , 3.Lab. Proteolytic Neuroscience, RIKEN Center for Brain Sci. )

Alzheimerʼs disease, App^{NL-G-F/NL-G-F} mouse, microglia

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The 42nd Annual Meeting of the Molecular Biology Society of Japan

[4P-0471] Deficiency of base excision repair enzyme, OGG1 or MUTYH alters activation status of microglia, amyloid-beta burden, and behavior pattern in App^NL-G-F knock-in mouse model of Alzheimerʼs disease

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The 42nd Annual Meeting of the Molecular Biology Society of Japan

[4P-0471] Deficiency of base excision repair enzyme, OGG1 or MUTYH alters activation status of microglia, amyloid-beta burden, and behavior pattern in AppNL-G-F knock-in mouse model of Alzheimerʼs disease

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[4P-0471] Deficiency of base excision repair enzyme, OGG1 or MUTYH alters activation status of microglia, amyloid-beta burden, and behavior pattern in App^NL-G-F knock-in mouse model of Alzheimerʼs disease