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Abstract
Increase in the quality of life, combined with drug strategies, has been studied as possibilities for improving memory and delaying the onset of neurodegenerative diseases. A previous study published by the group of the authors has shown that microdose lithium and enriched environment can improve memory in both mice and humans. To elucidate this relationship better, this study aimed to evaluate whether the chronic combination of these two strategies could increase healthy aging in Senescence Accelerated Mouse-Prone 8 (SAMP8). Animals were submitted to either one or both of these strategies until the age of 10 months when they were anesthetized and killed and their hippocampus was extracted. The untreated SAMP-8 group exhibited worse memory and reduced neuronal density with greater neurodegeneration and increased amyloid-β plaque density compared with the control group. Moreover, significant alterations in proteins related to long-term potentiation, such as, synaptophysin and brain-derived neurotrophic factor (BDNF), were observed in this group. The strategies used in the study maintained long-term memory, reduced anxiety, and increased neuroprotection. Both strategies were efficient in reducing neurodegeneration and increasing parameters related to memory maintenance. In many experiments, the combination of the two strategies was more effective in improving healthy aging. This study sheds light on the combination of strategies that choose to improve the quality of life and drugs with low side effects. Moreover, it opens perspectives for a new field of study for healthy aging.
Highlights
It is already known that increased longevity gives rise to chronic diseases that can be highly debilitating and influence the quality of life, as is the case of Alzheimer’s disease (AD)
To evaluate the spatial memory of senescenceaccelerated mice resistant (SAMR)-1 and Senescence Accelerated Mouse-Prone 8 (SAMP-8), animals were submitted to the Barnes maze for 5 consecutive days
A significant interaction between the factors time and strain [F(3,52) = 3.176, p < 0.05] was observed, as the SAMR1 group significantly increased their time spent in the right quadrant when the animals were re-exposed to the maze
Summary
It is already known that increased longevity gives rise to chronic diseases that can be highly debilitating and influence the quality of life, as is the case of Alzheimer’s disease (AD). LTP happens because of the synaptic activation of n-methyl-d-aspartate (NMDA) and α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors (Bliss and Collingridge, 1993). The activation of these receptors leads to an increase in intracellular calcium and activation of kinase proteins (Nicoll, 2017). The activation of calcium-calmodulin dependent protein kinase IV promotes the activation of the transcription factor cAMP-response element-binding protein (CREB) through phosphorylation (Finkbeiner, 2000; Mayr and Montminy, 2001; Kokubo et al, 2009), which increases neurotrophin synthesis. Brain-derived neurotrophic factor (BDNF) is one of these neurotrophins, and it plays a fundamental role in the consolidation of LTP (Finkbeiner, 2000; Mayr and Montminy, 2001; Kokubo et al, 2009)
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