9,49,50 The underlying mechanisms for these protective effects of caloric restriction, particularly the improvement in learning and memory in aged animals, includes changes in synaptic plasticity reduction in spine loss and increased neurogenesis in the hippocampus.51 The effects of caloric restriction on the brain, particularly the aging brain, are regionally specific and very much dependent on the neuronal and synaptic substrates of that specific area and its neuronal circuits.1 For example, it has been shown that the gray matter volume in the
caudate nucleus decreases with age in control animals, but is preserved in calorie-restricted monkeys.46 In contrast, other Inhibitors,research,lifescience,medical areas of the monkey brain, including the frontal and Selleckchem CDK inhibitor temporal cortex, are characterized by a significant reduction in Inhibitors,research,lifescience,medical gray matter volume that is not decreased by a reduction in food intake.46 Several studies have shown that caloric restriction elevates the levels of BDNF in several areas of the brain, particularly the hippocampus.51 These increases in BDNF levels seem to be regionally specific, as suggested by a recent study that evaluated the release of neurotransmitters and BDNF levels in rats subjected to Inhibitors,research,lifescience,medical a 40% restriction in food
intake throughout their entire lifespan.17 Caloric restriction may also be protective in Alzheimer’s disease and Parkinson’s disease, as well as in other neurodegenerative disorders.52,53 For instance, in mouse models of Alzheimer’s disease, caloric restriction has been shown to reverse the deficits in learning and memory typically found in these animals.54 Also, the motor impairment detected in a monkey model of Parkinson’s disease has been shown to be attenuated by caloric restriction.52 Inhibitors,research,lifescience,medical A major role of neurotrophic Inhibitors,research,lifescience,medical factors as well as other proteins and enzymes on these protective effects of caloric restriction has been suggested.9 Several studies highlight the role of certain nutrients for normal brain function, and
these nutrients may influence the activities of specific molecular substrates important for learning, memory, Ribonucleotide reductase and other cognitive functions.55 An example of one of those nutrients is the omega-3 fatty acids, which are considered essential for maintaining synaptic function and plasticity.55 In fact, the omega-3 fatty acid, docosahexaenoic acid, is an important component of neuronal membranes and it has been found that dietary supplementation with this fatty acid elevates the levels of BDNF in the hippocampus and counteracts rat learning disabilities after traumatic brain injury.56 Other micronutrients, such as vitamin E, have been shown to have the specific capacity to protect synaptic membranes from oxidative damage. Thus there are micronutrients that protect the brain against aging by promoting neuronal plasticity.