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More generally, we suggest that alterations in transmitter release, which disrupt neuronal communication throughout the brain (Dickstein et al., 2007) are likely to underlie variability in individual animal behavior and age-related cognitive and behavioral decline.
In this study, we used C. elegans male mating behavior to study the molecular and physiological alterations underlying the behavioral decline that occur during early aging.
In contrast, mTOR signaling was shown to be up-regulated in 7PA2 cells over-expressing mutant APP and in brains of another AD transgenic mouse, with rapamycin treatment reported as protective against behavioral decline [13], [14].
Epigallocatechin gallate (EGCG) did not extend C. elegans lifespan but attenuated the age-related behavioral decline [36] and extended survival rate under heat stress and oxidative stress by inducing SOD-3 and HSP-16.2 [37].
We also tested whether INS-1 (OE) could rescue aging-induced behavioral decline.
These results are consistent with the idea that ROS contributes to the behavioral decline.
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We tested the hypothesis that healthy older adults individuals who exhibit behavioral declines in relational memory would show reduced specificity of ventrolateral prefrontal and hippocampal regions during relational retrieval.
Sarcopenia, the loss of muscle mass, occurs in both humans and C. elegans as a result of advanced age and results in corresponding behavioral declines.
Our experiments show that experimental manipulations targeting neurotransmission pathways improve the aging-associated neuronal activity and olfactory behavioral declines.
Our experiments show that experimental manipulations aimed at increasing neurotransmitter release improve the aging-associated neuronal activity and behavioral declines.
Since behavior is largely affected by the functional state of the nervous system, age-related behavioral declines could very likely indicate the perturbations in the brain.
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