Method: Seventeen female transgenic mice overexpressing human amyloid precursor protein (APP) with Swedish and Indiana mutations (J20, 6 months old) were divided into the experimental (EX, n = 10) and control (C, n = 7) groups. In the EX group, maxillary bilateral molar teeth were extracted at 6 months of birth, but they remained intact in the C group. After 6 and 10 months of extraction, passive avoidance test was performed to evaluate learning and memory. After the test at 10 months, the mice were killed and their brains removed. Amyloid beta protein (Aβ) deposition and change of neuronal cell numbers in the hippocampus were investigated in half of the brain of each mouse. The other half of brain was homogenized, and the Aβ40 and Aβ42 levels were quantified using ELISA. The obtained data were analyzed by using Student’s t test and Fisher’s exact test.
Result: Learning and memory were significantly impaired in the EX group than the C group (p ‹ 0.05) at 10 months. The neuronal cell number in the CA1 and CA3 regions of the hippocampus was significantly decreased in the EX group (CA1: 89.1 ± 3.9 ; CA3: 80.0 ± 3.1) than the C group (CA1: 101.0 ± 3.9 ; CA3: 91.0 ± 6.0) (p ‹ 0.05). The levels of total Aβ, Aβ40, and Aβ42 showed no intergroup difference.
Conclusion: These lines of evidence suggest that molar tooth loss may cause neuronal cell loss in the hippocampus, leading to memory impairment, and that the amyloid cascade may not be involved in these events.