Occlusal disharmony transiently decrease cognition via cognitive suppressor molecules and partially restores cognitive ability via clearance molecules.

Occlusal disharmony has been reported to be affected not only by cytokine and steroid hormone secretion and sympathetic activation in peripheral organs, but also by neurotransmitter release in the central nervous system. However, little is known about whether occlusal disharmony can decrease cognitive ability. We hypothesized that hyperocclusion decreases cognition via Alzheimer's disease-associated molecule expression in the brain. The present study is aimed to elucidate the relationships among occlusal disharmony, cytokine and cognitive-regulated molecule expression in the brain, and the impairment of learning and memory cognition. We examined the effect of hyperocclusion on the relationships among cytokine expression, cognitive suppressor molecules in the hippocampus, and cognition in behavior using a hyperocclusion mouse model. Hyperocclusion dramatically increased interleukin-1ß expression in the serum and hippocampus 1 week after hyperocclusal loading in 2-month-old mice, but no effects in 12-month-old mice. The social and long-term cognitive abilities of the 2-month-old mice were transiently downregulated close to the level of the 12-month-old mice 1 week after hyperocclusion and recovered to close to basal level via the expression of cognitive suppressor clearing proteins. The expression levels of amyloid-ß and phosphorylated tau were significantly upregulated 1 week after hyperocclusal loading in the hippocampus of 2-month-old mice but were constant in 12-month-old mice. Occlusal disharmony-induced interleukin-1ß expression may contribute to accumulation of cognitive suppressor molecules such as amyloid-ß and phosphorylated tau and activate their clearance proteins, resulting in protection against transient dementia in young but not older individuals.

Initial hydraulic failure followed by late-stage carbon starvation leads to drought-induced death in the tree Trema orientalis.

Drought-induced tree death has become a serious problem in global forest ecosystems. Two nonexclusive hypotheses, hydraulic failure and carbon starvation, have been proposed to explain tree die-offs. To clarify the mechanisms, we investigated the physiological processes of drought-induced tree death in saplings with contrasting Huber values (sapwood area/total leaf area). First, hydraulic failure and reduced respiration were found in the initial process of tree decline, and in the last stage carbon starvation led to tree death. The carbohydrate reserves at the stem bases, low in healthy trees, accumulated at the beginning of the declining process due to phloem transport failure, and then decreased just before dying. The concentrations of non-structural carbohydrates at the stem bases are a good indicator of tree damage. The physiological processes and carbon sink-source dynamics that occur during lethal drought provide important insights into the adaptive measures underlying forest die-offs under global warming conditions.