Volume 23, Issue 3 (Autumn 2021)
Advances in Cognitive Sciences 2021, 23(3): 1-13 |
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1- Medical Student, Student Research Committee, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
2- Associate Professor of Physiology, Neuroscience Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
3- Associate Professor of Physiology, Physiology Department, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
2- Associate Professor of Physiology, Neuroscience Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
3- Associate Professor of Physiology, Physiology Department, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
Abstract: (2168 Views)
Introduction
The main goal in treating diseases that cause memory dysfunction is to improve the condition or prevent the progression of memory and cognition impairment (1). Non-pharmacological treatments such as behavioral therapy, fact-finding, art therapy, music therapy, phototherapy, interpersonal therapy, and occupational therapy are also used for these diseases (2). The first attempt at studying the effect of enhanced environments on animals was made by the Italian Malacarne (1744-1844) (8). According to Malacarne, birds in enriched cages have larger brain volumes than birds in simple cages (8). In the 1960s, enriched environment (EE) was used as a scientific model, and its first neuroanatomical effect was studied in Berkeley's psychology lab (12). The EE as a non-pharmacological treatment can improve the living conditions of the laboratory animals compared to the animals in a standard cage by increasing social, cognitive, and physical stimuli (13). The EE is typically a large cage with various toys, tunnels, ladders for exploration, and a running wheel for training. Manipulating the normal environment by placing the devices as mentioned above or moving objects in a cage will change the social and physical environment and increase animals’ cognition levels. Also, EEs can include hidden food pellets and various snacks placed in the toys to encourage animals to search and obtain food. This type of EE gives animals a special ability to control their environment and essential resources (13-15). It is generally believed that being in an EE for 3 to 6 weeks is enough to reduce learning and memory deficits in old rodents (20). It has been shown that lifelong exposure to the EE can have much stronger and more effective beneficial effects (21). Exposure to complex and enriched environments causes significant changes in brain weight, especially in the cerebral cortex and hippocampus thickness and weight (23). Over the last few years, the impact of living in an EE on cognitive development has been one of the hottest topics (5). Obviously, neurogenesis plays a crucial role in cognitive ability, as well as emotional behavior, which are both related to hippocampal function (27). It has been shown that EE increases the survival of new proliferating hippocampal granular neurons (28). The EE not only changes the number of neurons, but also alters the morphology of nerve cells, and increases the number of dendritic branches and spines (29). Given that dendritic spines are the site of synaptic connections; it seems that synapses number increment is one of the main mechanisms to improve the cognitive status of the EE inhabitant animals. Even if the newly formed spines do not form functional synapses, they may still serve as a source of synapses that can be activated during stimulation, which would lead to, faster learning of rodents in enriched environments than rodents in standard environments (30). The increase of neurotrophic factors such as brain-derived neurotrophic factor, insulin-like growth factor-1, and nerve growth factor level is another mechanism that can be considered as motor and cognitive improvement followed by the presence in the EE. These factors may increase in different brain areas, including the cerebral cortex, hippocampus, and cerebellum (35-38). Another probable effective mechanism is the EE effect on synaptic neurotransmission (39). It has been suggested that EE can increase the number of N-methyl-d-aspartate (NMDA) receptors in the rat hippocampus. Also, learning and memory improvement due to increased presynaptic NMDA receptors and the subsequent increase of norepinephrine secretion have been reported for the mice inhabited in the EE (44,45). Furthermore, it has been proved that cholinergic synaptic transmission is raised in the EE inhabited mice (45). The EE plays an important role in learning, memory, and cognition improvement by way of increasing the number of α-7 receptors, which are often located in the CA1 region of the hippocampus (46). Moreover, the EE reduces the amount of acetylcholinesterase in the amygdala and also increases epinephrine in the experimental animal's brain (44). Furthermore, the EE increases dopamine level (48) in the amygdala and hippocampus of mice, along with increasing the number of serotonin receptors in the hippocampus (49). At the same time, the role of EE in preventing neurological disorders and neuro-inflammation has also been investigated. The obtained shreds of evidence suggest that behavioral interventions, which allow new neurons to survive, may protect us against Alzheimer's disease (52). The neurogenic storage hypothesis states that EE can stimulate neurogenesis and allow the hippocampus to adapt properly to environmental damage (27). Inflammation in the hippocampus decreases the expression of brain-derived growth factors and nerve growth factors by increasing the expression of pro-inflammatory cytokines, including interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha (59). The EE reduces the production of inflammatory cytokines and, on the other hand, increases the production of anti-inflammatory cytokines in the hippocampus to prevent the progression of neuro-inflammatory processes. Additionally, by increasing angiogenesis in the brain, the EE facilitates the elimination of harmful agents produced by neuroinflammation (15, 60).
Methods
This study was conducted to review the world's research literature on EE and its effects on memory and cognitive disorders. A review of the keywords: Enriched Environment, Memory, and Cognitive Impairment in the title and abstract of articles published in reputable international scientific databases were searched. Finally, after several steps of removing duplicate and unrelated items, 69 articles were used.
Results
Different types of enriched environments create sensory, motor, social and cognitive stimuli for animals and can affect and improve their cognitive and behavioral abilities in different ways. It is better to encourage animals to search and play than an EE includes wheelchairs, colored objects, tunnels, ladders, mirrors, and hidden food pellets along with increasing the cage size and number of animals. Animals that live in such an environment have a remarkable ability to control their environment and essential resources. However, it should be noted that all enriched environments did not improve animal’s cognition or welfare; for example, in some strains of mice, it has been shown that many stimuli can lead to anxiety and/or aggressive behavior.
Conclusion
In contrast to pharmacological interventions, behavioral treatments and an active lifestyle have shown encouraging benefits, and even in the elderly, they are more convenient to avoid the overconsumption of medicine, which is one of the typical characteristics of their age. Behavioral therapies like EE have had positive results in the prevention and treatment of cognitive impairments in animals. Although all benefits of EE in laboratory models are great, it will be challenging to apply it to human diseases if we do not understand how it affects humans. However, the efficacy of EE alongside medication for treating some pediatric diseases has been anecdotally shown. Having the fact that EE can reduce the occurrence of cognitive disorders, there are still many questions regarding it, which require clinical trials to clarify.
Ethical Considerations
Compliance with ethical guidelines
All ethical principles were observed.
Authors’ contributions
All three authors were involved in the design and formulation of the argument.
Funding
This article is written at personal expense.
Acknowledgments
No need.
Conflict of interest
There is no conflict of interest
The main goal in treating diseases that cause memory dysfunction is to improve the condition or prevent the progression of memory and cognition impairment (1). Non-pharmacological treatments such as behavioral therapy, fact-finding, art therapy, music therapy, phototherapy, interpersonal therapy, and occupational therapy are also used for these diseases (2). The first attempt at studying the effect of enhanced environments on animals was made by the Italian Malacarne (1744-1844) (8). According to Malacarne, birds in enriched cages have larger brain volumes than birds in simple cages (8). In the 1960s, enriched environment (EE) was used as a scientific model, and its first neuroanatomical effect was studied in Berkeley's psychology lab (12). The EE as a non-pharmacological treatment can improve the living conditions of the laboratory animals compared to the animals in a standard cage by increasing social, cognitive, and physical stimuli (13). The EE is typically a large cage with various toys, tunnels, ladders for exploration, and a running wheel for training. Manipulating the normal environment by placing the devices as mentioned above or moving objects in a cage will change the social and physical environment and increase animals’ cognition levels. Also, EEs can include hidden food pellets and various snacks placed in the toys to encourage animals to search and obtain food. This type of EE gives animals a special ability to control their environment and essential resources (13-15). It is generally believed that being in an EE for 3 to 6 weeks is enough to reduce learning and memory deficits in old rodents (20). It has been shown that lifelong exposure to the EE can have much stronger and more effective beneficial effects (21). Exposure to complex and enriched environments causes significant changes in brain weight, especially in the cerebral cortex and hippocampus thickness and weight (23). Over the last few years, the impact of living in an EE on cognitive development has been one of the hottest topics (5). Obviously, neurogenesis plays a crucial role in cognitive ability, as well as emotional behavior, which are both related to hippocampal function (27). It has been shown that EE increases the survival of new proliferating hippocampal granular neurons (28). The EE not only changes the number of neurons, but also alters the morphology of nerve cells, and increases the number of dendritic branches and spines (29). Given that dendritic spines are the site of synaptic connections; it seems that synapses number increment is one of the main mechanisms to improve the cognitive status of the EE inhabitant animals. Even if the newly formed spines do not form functional synapses, they may still serve as a source of synapses that can be activated during stimulation, which would lead to, faster learning of rodents in enriched environments than rodents in standard environments (30). The increase of neurotrophic factors such as brain-derived neurotrophic factor, insulin-like growth factor-1, and nerve growth factor level is another mechanism that can be considered as motor and cognitive improvement followed by the presence in the EE. These factors may increase in different brain areas, including the cerebral cortex, hippocampus, and cerebellum (35-38). Another probable effective mechanism is the EE effect on synaptic neurotransmission (39). It has been suggested that EE can increase the number of N-methyl-d-aspartate (NMDA) receptors in the rat hippocampus. Also, learning and memory improvement due to increased presynaptic NMDA receptors and the subsequent increase of norepinephrine secretion have been reported for the mice inhabited in the EE (44,45). Furthermore, it has been proved that cholinergic synaptic transmission is raised in the EE inhabited mice (45). The EE plays an important role in learning, memory, and cognition improvement by way of increasing the number of α-7 receptors, which are often located in the CA1 region of the hippocampus (46). Moreover, the EE reduces the amount of acetylcholinesterase in the amygdala and also increases epinephrine in the experimental animal's brain (44). Furthermore, the EE increases dopamine level (48) in the amygdala and hippocampus of mice, along with increasing the number of serotonin receptors in the hippocampus (49). At the same time, the role of EE in preventing neurological disorders and neuro-inflammation has also been investigated. The obtained shreds of evidence suggest that behavioral interventions, which allow new neurons to survive, may protect us against Alzheimer's disease (52). The neurogenic storage hypothesis states that EE can stimulate neurogenesis and allow the hippocampus to adapt properly to environmental damage (27). Inflammation in the hippocampus decreases the expression of brain-derived growth factors and nerve growth factors by increasing the expression of pro-inflammatory cytokines, including interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha (59). The EE reduces the production of inflammatory cytokines and, on the other hand, increases the production of anti-inflammatory cytokines in the hippocampus to prevent the progression of neuro-inflammatory processes. Additionally, by increasing angiogenesis in the brain, the EE facilitates the elimination of harmful agents produced by neuroinflammation (15, 60).
Methods
This study was conducted to review the world's research literature on EE and its effects on memory and cognitive disorders. A review of the keywords: Enriched Environment, Memory, and Cognitive Impairment in the title and abstract of articles published in reputable international scientific databases were searched. Finally, after several steps of removing duplicate and unrelated items, 69 articles were used.
Results
Different types of enriched environments create sensory, motor, social and cognitive stimuli for animals and can affect and improve their cognitive and behavioral abilities in different ways. It is better to encourage animals to search and play than an EE includes wheelchairs, colored objects, tunnels, ladders, mirrors, and hidden food pellets along with increasing the cage size and number of animals. Animals that live in such an environment have a remarkable ability to control their environment and essential resources. However, it should be noted that all enriched environments did not improve animal’s cognition or welfare; for example, in some strains of mice, it has been shown that many stimuli can lead to anxiety and/or aggressive behavior.
Conclusion
In contrast to pharmacological interventions, behavioral treatments and an active lifestyle have shown encouraging benefits, and even in the elderly, they are more convenient to avoid the overconsumption of medicine, which is one of the typical characteristics of their age. Behavioral therapies like EE have had positive results in the prevention and treatment of cognitive impairments in animals. Although all benefits of EE in laboratory models are great, it will be challenging to apply it to human diseases if we do not understand how it affects humans. However, the efficacy of EE alongside medication for treating some pediatric diseases has been anecdotally shown. Having the fact that EE can reduce the occurrence of cognitive disorders, there are still many questions regarding it, which require clinical trials to clarify.
Ethical Considerations
Compliance with ethical guidelines
All ethical principles were observed.
Authors’ contributions
All three authors were involved in the design and formulation of the argument.
Funding
This article is written at personal expense.
Acknowledgments
No need.
Conflict of interest
There is no conflict of interest
Received: 2021/04/26 | Accepted: 2021/06/29 | Published: 2021/11/16
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