The Aging Brain: Cognitive Decline and the Role of Diet
Aging is currently a hot topic among researchers. There may be several reasons for this; however, one of the clearest is the distinct molecular and cognitive alterations in the aging brain. As organisms age, the molecular structure of the brain display changes such as the accumulation of proteins, lipids, and other molecules that interfere with the normal functioning of the brain (Van houcke et al., 2015). Some studies demonstrated that neuronal loss in the brain in aged organisms contribute to cognitive decline as well as other molecular changes (Kovacs et al., 2014). However, there are other findings that suggest that there is not a significant neuronal loss in the aging brain, but rather a change in the number and structure of the synapses (Shi et al., 2007). Thus, the role of neuronal loss in cognitive decline in the aging brain is controversial. As a result of these and other molecular alterations, there are significant decreases/changes in cognitive abilities such as problem-solving, information processing, decision-making, speed of processing, executive function, and memory as aging occurs (Klimova et al., 2017; Murman, 2015). These abilities are crucial for individuals’ normal functioning in everyday life; therefore, it is important to investigate the underlying physiological mechanisms of cognitive abilities and the factors that lead to impairment in these.
One of the most important of these cognitive functions is clearly memory. Learning and memory mechanisms are significantly affected by aging, and these changes lead to a decrease in quality of life among older individuals (Arslan-Ergul et al., 2013). Several studies showed that there are gray matter volume decreases in the frontal regions of the brains of elderly individuals (Raz, 2000). Goldman-Rakic and Brown (1981) demonstrated dopamine reduction in the frontal lobes of aging monkey models which was proposed to contribute to cognitive decline. Such findings make it clear that there are several structural and molecular changes that contribute to learning and memory impairment in the aging brain. Learning and memory impairments are also present in aging-related diseases such as Alzheimer’s disease. In fact, progressive memory loss is a key feature of Alzheimer’s disease; and it may lead to other problems such as depression, speech impairments, and dependence on others (Newman et al., 2010). It is now clear that Alzheimer’s disease is characterized by the accumulation of amyloid and tau proteins, which also contributes to our knowledge that impaired molecular mechanisms are likely to be involved in learning and memory deficits. In order to improve the quality of life of elderly people with learning and memory problems, the mechanisms of these cognitive changes, and factors that lead to their impairment as well as factors that promote them need to be investigated.
As hinted above, there are many mechanisms, pathways, and biomolecules involved in learning and memory processes. The main mechanism of learning is long-term potentiation (LTP), which is a process by which the continuously stimulated synapses are strengthened by the activation of NMDA and AMPA receptors through the neurotransmitter glutamate (Bliss & Collingridge, 1993). LTP is thought to be the main process for learning and memory formation; therefore, it is significant in learning and memory research. One of the molecules that are thought to be significant in LTP is a brain-derived neurotrophic factor (BDNF) (Leal et al., 2016). BDNF is believed to be regulating the synapse formation during LTP. Multiple studies have investigated the relationship between BDNF and LTP. One of these studies found that when one allele of the BDNF gene was deleted, the mice showed significant impairment in LTP induction (Bartoletti et al., 2002). Similarly, it has been reported that there are decreased levels of BDNF in Alzheimer’s disease (Spencer, 2008). Apart from learning, BDNF has also been implicated in long-term memory processes. In rodents, one of the brain regions with the highest BDNF expression is the hippocampus, which is a structure crucial in memory formation (Kawamoto et al., 1996). Minichiello et al. (1999) demonstrated that mice with knockout TrkB gene, which is responsible for the production of a BDNF receptor TrkB, show impairment in learning and memory. Another study found that BDNF infusion in the hippocampus reversed the memory deficits in rats; and that BDNF may be responsible for the persistence of long-term memories (Bekinschtein et al., 2007). All of these findings indicate that BDNF plays a crucial role in learning and memory processes; therefore, it is likely significant to investigate them in aging organisms.
The role of diet in cognitive aging
Environmental factors such as intellectual engagement, physical training, and diet influence cognitive aging; specifically learning and memory (Kramer et al., 2004; Arslan-Ergul et al., 2013). There are many studies focusing especially on the role of diet in cognitive aging. Caloric restriction (CR) is one of the main focuses of research: Adams et al. (2008) found that CR prevents/reduces age-related decline in spatial learning ability in the middle- and old-aged rats. Similarly, Park et al. (2013) demonstrated that long-term exposure to CR increased the number of proliferating neural cells in mice. Positive effects of CR were also observed in age-related NMDA and AMPA receptor decline. Shi et al. (2007) showed that CR prevents the age-related loss of NMDA and AMPA subunits by stabilizing them. Apart from caloric restriction, diet research on cognitive aging focuses on the effects of different nutrients on cognitive functions. One major group of nutrients that are investigated in terms of brain aging is dietary polyphenols.
Polyphenols are antioxidants that are naturally present in many of the foods that we consume such as tea, wine, coffee, grapes, berries, and other types of fruits, vegetables, and beverages (Singh et al., 2008). Research indicates that dietary intake of these antioxidants may have different benefits in terms of cognitive functioning. Spencer (2009) argues that dietary intake of flavonoids, which is a subgroup of polyphenols, increased rats’ spatial memory measured by water maze tasks. Another study found that hippocampal BDNF activity increases when rats were supplemented with blueberries (Williams et al., 2008). Richetti et al. (2011) demonstrated that zebrafish that were injected with the flavonoids quercetin or rutin before the induction of scopolamine showed no scopolamine-induced memory deficits. Interestingly, one study demonstrated that a flavonoid of citrus peels lowered Aβ accumulation and amyloid-induced memory deficit in rat models (Onozuka et al., 2008). In light of all the evidence above, it would be safe to conclude that environmental factors, specifically diet, play a crucial role in cognitive function. Therefore, diet can be manipulated to investigate the effects of caloric restriction or specific nutrients on cognitive aging, especially learning and memory.
Conclusion
The aim of this review was to point to the relationship between some of the factors that play a role in the cognitive functions of the aging brain- especially learning and memory. I wanted to talk about diet specifically because the diet is the biggest and most easily accessible part of our daily lives. We need to understand the role that diet and other factors play in learning and memory (and cognition) in order to maintain a healthy mind as we age.
