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Published on: February 6, 2019
Occlusal disharmony transiently decrease cognition via cognitive suppressor molecules and partially restores
Munehisa Maeshiba1, Hiroshi Kajiya2, Takashi Tsutsumi3
1Oral Medicine Research Center, Fukuoka Dental College, Fukuoka, Japan; Department of Oral Rehabilitation, Fukuoka Dental College, Fukuoka, Japan.
Hyperocclusion in young mice transiently impairs cognition by increasing Alzheimer's-associated proteins. This effect is mediated by interleukin-1β and reversed by clearance proteins, offering temporary protection against cognitive decline.
Area of Science:
- Neuroscience
- Oral Health
- Immunology
Background:
- Occlusal disharmony is linked to systemic physiological changes, including hormonal and neural alterations.
- The impact of occlusal disharmony on cognitive function, particularly learning and memory, remains poorly understood.
- Alzheimer's disease-associated molecules are implicated in cognitive regulation.
Purpose of the Study:
- To investigate the hypothesis that hyperocclusion (excessive biting force) impairs cognition through the expression of Alzheimer's disease-associated molecules in the brain.
- To elucidate the relationship between occlusal disharmony, central nervous system cytokine and cognitive-regulated molecule expression, and learning/memory deficits.
Main Methods:
- A hyperocclusion mouse model was utilized to assess the effects on cytokine expression, hippocampal cognitive suppressor molecules, and behavioral cognition.
- Mice of two age groups (2-month-old and 12-month-old) were subjected to hyperocclusal loading.
- Measurements included serum and hippocampal interleukin-1β, amyloid-β, phosphorylated tau, and cognitive suppressor clearing proteins, alongside behavioral tests.
Main Results:
- Hyperocclusion significantly increased interleukin-1β in young (2-month-old) mice's serum and hippocampus within one week, with no effect in older (12-month-old) mice.
- Young mice exhibited transiently reduced social and long-term cognitive abilities post-hyperocclusion, which recovered through the expression of cognitive suppressor clearing proteins.
- Amyloid-β and phosphorylated tau levels were elevated in the hippocampus of young mice after hyperocclusion, but remained unchanged in older mice.
Conclusions:
- Occlusal disharmony-induced interleukin-1β may drive the accumulation of cognitive suppressors like amyloid-β and phosphorylated tau.
- The brain activates clearance proteins to counteract these molecules, providing transient protection against cognitive impairment in young individuals.
- Older individuals do not exhibit the same protective response, suggesting age-dependent vulnerability to occlusal disharmony-related cognitive changes.
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