1. Tooth loss early in life induces hippocampal morphology remodeling in senescence-accelerated mouse prone 8 (SAMP8) mice
- Author
-
Masahisa Katano, Kyoko Kajimoto, Kagaku Azuma, Kin-ya Kubo, and Mitsuo Iinuma
- Subjects
Male ,Senescence ,Aging ,medicine.medical_specialty ,Time Factors ,hippocampus ,Neurogenesis ,Spatial Learning ,Hippocampus ,Biology ,Hippocampal formation ,Lipofuscin ,Synapse ,Mice ,Tooth Loss ,03 medical and health sciences ,myelin sheath ,0302 clinical medicine ,Microscopy, Electron, Transmission ,stomatognathic system ,synapse ,Internal medicine ,transmission electron microscopy ,Tooth loss ,medicine ,Animals ,Body Weight ,Post-Synaptic Density ,General Medicine ,Molar ,Axons ,Mitochondria ,Disease Models, Animal ,stomatognathic diseases ,Endocrinology ,Synapses ,Ultrastructure ,Dementia ,030211 gastroenterology & hepatology ,medicine.symptom ,Cognition Disorders ,Corticosterone ,Postsynaptic density ,Research Paper - Abstract
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.
- Published
- 2020