Tooth loss early in life induces hippocampal morphology remodeling in senescence-accelerated mouse prone 8 (SAMP8) mice

被引:15
作者
Katano, Masahisa [1 ]
Kajimoto, Kyoko [1 ]
Iinuma, Mitsuo [1 ]
Azuma, Kagaku [2 ]
Kubo, Kin-ya [3 ]
机构
[1] Asahi Univ, Dept Pediat Dent, Sch Dent, 1851 Hozumi, Mizuho, Gifu 5010296, Japan
[2] Univ Occupat & Environm Hlth, Sch Med, Dept Anat, Yahatanishi Ku, 1-1 Iseigaoka, Kitakyushu, Fukuoka 8078555, Japan
[3] Nagoya Womens Univ, Grad Sch Human Life Sci, Mizuho Ku, 3-40 Shioji Cho, Nagoya, Aichi 4678610, Japan
关键词
tooth loss; hippocampus; transmission electron microscopy; mitochondria; myelin sheath; synapse; NEUROTROPHIC FACTOR; MEMORY DEFICIT; DENTATE GYRUS; MODEL; IMPAIRMENT; EXPRESSION; STRESS; PROLIFERATION; NEUROGENESIS; INVOLVEMENT;
D O I
10.7150/ijms.40241
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Long-term tooth loss is associated with the suppression of hippocampal neurogenesis and impairment of hippocampus-dependent cognition with aging. The morphologic basis of the hippocampal alterations, however, remains unclear. In the present study, we investigated whether tooth loss early in life affects the hippocampal ultrastructure in senescence-accelerated mouse prone 8 (SAMP8) mice, using transmission electron microscopy. Male SAMP8 mice were randomized into control or tooth-loss groups. All maxillary molar teeth were removed at 1 month of age. Hippocampal morphologic alterations were evaluated at 9 months of age. Tooth loss early in life induced mitochondrial damage and lipofuscin accumulation in the hippocampal neurons. A thinner myelin sheath and decreased postsynaptic density length were also observed. Our results revealed that tooth loss early in life may lead to hippocampal ultrastructure remodeling and subsequent hippocampus-dependent cognitive impairment in SAMP8 mice with aging.
引用
收藏
页码:517 / 524
页数:8
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