مروری بر محیط غنی و اثرات آن بر یادگیری، حافظه و اختلالات شناختی

مقدمه: با توجه به عدم وجود درمان‌های قطعی برای اختلالات شناختی، پژوهشگران در مطالعات مختلف به ارائه‌ روش‌های جدید به منظور بهبود نسبی و یا جلوگیری از تشدید اختلالات حافظه و شناخت به منظور کاهش وابستگی بیمار به دیگران تمرکز نموده‌اند. یکی از درمان‌های غیر دارویی که در مطالعات حیوانی جهت بهبود اختلالات شناختی مورد توجه قرار گرفته است، محیط غنی می‌باشد. محیط غنی اشاره به محیطی دارد که تحریکات اجتماعی، شناختی، و فیزیکی را برای یک موجود فراهم می آورد. در این مقاله‌ مروری به چگونگی تاثیر محیط غنی بر اختلالات شناختی و مکانیسم‌های دخیل در آن پرداخته شده است. لذا این مطالعه با هدف مروری بر مقالات انگلیسی پیرامون محیط غنی و تاثیر آن بر حافظه و اختلالات شناختی انجام شد.روش کار: در این مقاله کلید ‌واژه‌هایenriched environment ، memory و cognitive impairment در عنوان و چکیده مقالات چاپ شده در پایگاه‌های علمی معتبر بین المللی مورد جستجو قرار گرفت. پس از چند مرحله حذف موارد تکراری و غیر مرتبط در نهایت از 69 مقاله استفاده شد. یافته‌ها: محیط غنی می‌تواند به واسطه‌ ایجاد مجموعه‌ای از تحریکات حسی، حرکتی، اجتماعی و شناختی، موجب بهبود حافظه و روندهای شناختی شود. تغییرات ایجاد شده می‌تواند به دلیل تاثیرات گوناگونی باشد که حضور در محیط غنی بر تعداد نورون‌ها، مورفولوژی نورون ‌ها، میلین ‌سازی، سیناپس‌ها و انتقال دهنده‌های عصبی، عوامل نوروتروفیک و التهاب عصبی دارد. نتیجه‌گیری: با توجه به نقش محیط غنی در بهبود اختلالات مولکولی و عملکردی سیستم عصبی مرکزی در بیماری ‌هایی مانند افسردگی و سکته مغزی و کاهش خطر ابتلا به زوال عقل در انسان؛ می‌توان امیدوار بود تا در آینده نزدیک محیط غنی به معنی فراهم آوردن محیط زندگی مناسب و دلپذیر به عنوان یک راهکار غیر دارویی موثر در درمان بیماری‌های تحلیل برنده عصبی در انسان مورد استفاده قرار گیرد.

A review of the enriched environment and its effects on learning, memory and cognitive disorders

IntroductionThe main goal in treating diseases that cause memory dysfunction is to improve the condition or prevent the progression of memory and cognition impairment (1). Nonpharmacological treatments such as behavioral therapy, factfinding, 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 (17441844) (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 #39;s psychology lab (12). The EE as a nonpharmacological 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 rsquo; 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 (1315). 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 brainderived neurotrophic factor, insulinlike growth factor1, 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 (3538). Another probable effective mechanism is the EE effect on synaptic neurotransmission (39). It has been suggested that EE can increase the number of Nmethyldaspartate (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 alpha;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 #39;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 neuroinflammation has also been investigated. The obtained shreds of evidence suggest that behavioral interventions, which allow new neurons to survive, may protect us against Alzheimer #39;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 brainderived growth factors and nerve growth factors by increasing the expression of proinflammatory cytokines, including interleukin1 beta, interleukin6, and tumor necrosis factoralpha (59). The EE reduces the production of inflammatory cytokines and, on the other hand, increases the production of antiinflammatory cytokines in the hippocampus to prevent the progression of neuroinflammatory processes. Additionally, by increasing angiogenesis in the brain, the EE facilitates the elimination of harmful agents produced by neuroinflammation (15, 60).MethodsThis study was conducted to review the world #39;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.ResultsDifferent 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 rsquo;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.ConclusionIn 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 ConsiderationsCompliance with ethical guidelines All ethical principles were observed.Authors rsquo; contributionsAll three authors were involved in the design and formulation of the argument.FundingThis article is written at personal expense.AcknowledgmentsNo need.Conflict of interestThere is no conflict of interest