Hoiland E. Brain plasticity: What is it? Chudler EH, ed. Neuroscience for Kids. University of Washington. James W. The Principles of Psychology. Classics in the History of Psychology. Green CD, ed. Kolb B, Gibb R. Brain plasticity and behaviour in the developing brain. Clarke M, Ghali L, eds. Your Privacy Rights. To change or withdraw your consent choices for VerywellMind.
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Send assessments and training programs to your children or other family members. Send assessments and training programs to research participants. Although this term is now commonly used in psychology and neuroscience, it is not easily defined and is used to refer to changes at many levels in the nervous system ranging from molecular events, such as changes in gene expression, to behavior.
Neuroplasticity, or neural plasticity, allows neurons to regenerate both anatomically as well as functionally, and to form new synaptic connections. Brain plasticity, or neuroplasticity, is the ability for the brain to recover and restructure itself.
This adaptive potential of the nervous system allows the brain to recover after disorders or injuries and to reduce the effects of altered structures due to pathologies such as Multiple Sclerosis, Parkinson's disease, cognitive deterioration, Alzheimer's, dyslexia, ADHD, insomnia, etc.
Neural networks before training Neural networks 2 weeks after stimulation Neural networks 2 months after stimulation.
When engaged in new experiences and learning, the brain establishes a series of neural pathways. These neural pathways, or circuits, are routes made of inter-connecting neurons. The intrinsic factors that are least likely to be modified in the process of aging are neuroinflammation, oxidative stress, and brain injury and other factors such as lifestyle that can be modified for slowing the aging process is a low intake of fat and sugar diets and alcohol and avoid opioid addictions [ 2 ].
One of the diet modifications can be done by adding polyphenols e. Even though polyphenols are not considered essential nutrients, these compounds can decrease the risk of age-related cognitive problems. The food which contains an abundant number of macronutrients like omega-3 fatty acids omega-6 poly-unsaturated fatty acids and flavonoids are found in vegetables, fish, and nuts that develop a favorable environment for the brain to generate new connections and synapsis and make that synapsis strong [ 1 - 4 ].
Polyphenols play vital roles in neuroplasticity, neurogenic, anti-inflammatory, and neuroprotective effects, especially this effect is observed with curcumin, catechins, resveratrol, and omega-3 fatty acids [ 4 ].
Curcumin: Curcumin is a plant-based diarylheptanoid that produces yellow pigment mostly used in curries as it can modulate various signaling properties because of its polyphenol properties. It has anti-inflammatory, anti-bacterial, cytotoxic, antioxidant proliferative, wound healing, and anti-nociceptive properties [ 12 , 13 ].
Curcumin has antioxidant and free-radical properties, which have been shown in various studies. The phenolic hydroxyl group of curcumin has antioxidant activity that is produced endogenously including superoxide dismutase SOD , catalases, peroxiredoxins, and glutathione, which play critical roles in preventing endogenous and xenobiotic-induced oxidative damage [ 13 ]. Also in another study, it states anti-oxidant therapy is not enough to prevent age-related neurodegenerative disorder.
They mentioned the removal of oxidative deterioration by scavenging oxidants [ 14 ]. Curcumin can bind in amyloid-beta protein, it's fluorescent property can help in early detection of Alzheimer's disease [ 15 ]. The development of the more powerful aggregation inhibitor 3-[ 1E 1H-indolyl ethenyl][ 1E [2-methoxy 2-pyridylmethoxy phenyl] ethenyl]-1H-pyrazole compound four has a better pharmacokinetic profile and pharmacological efficacy in vivo than curcumin, making it also suitable for the age-related degenerative disease [ 16 ].
Curcumin is a polyphenol that is one of the chief spices of Asian cuisine. The benefit of curcumin has been examined extensively, which shows the potential benefit of healthy brain growth and also the process of neurogenesis [ 17 ]. Aged Sprague-Dawley rats age 15 months; male were given a 0. Rats showed improved performance on an olfactory cortex-based social recognition memory task at both six and twelve weeks, and on hippocampus-dependent spatial learning and memory task after 12 weeks, relative to controls.
The rats that were administered curcumin showed increased proliferation in the dentate gyrus DG at 12 weeks, relative to diet controls, which show the process of neurogenesis in the olfactory cortex [ 18 ]. The vital role of neurogenesis has been played not only in animals but also in humans. The association between curry consumption and cognitive function is studied in a large group of the elderly non-demented population.
The study revealed those population which used curcumin in their diet frequently scored finding that persons who frequently consumed curry scored meaningfully well on the Mini-Mental State Examination comparatively to those who irregularly consumed curry. The next study of a six-month randomized, placebo-controlled, double-blind, clinical study of curcumin in persons with progressive cognitive decline and memory found elevated serum amyloid beta, but not improvements on the Mini-Mental State Examination [ 17 ].
Various studies provide the evidence in its neurogenesis with curcumin; however, none of the studies precisely identified as what causes a person to maintain a neuronal growth with the use of this spice. The chief drawback of curcumin to be used as medicine is its poor bioavailability. If the scientist and researcher can modify curcumin in such a way that a vast amount is absorbed, then it would be more straightforward to assess the effect of this yellow pigment.
More studies are still required to be conducted to identify its effect on brain growth and soon will be able to use this ingredient in the medicine to prevent neurodegenerative disease. Dietary Energy Restriction: The hypothalamus of the brain regulates a dietary intake calorie ; that is why it is believed to deliver a significant impact in the brain by the diet we consume.
Multiple studies have been undertaken in rats and mice, and the evidence from them shows sustained excessive energy intake can adversely affect the cognitive function of the brain. Excessive energy intake can result to decrease cognitive function, increase the risk of age-related disorders.
It makes neurons vulnerable to aging, and neurodegenerative disorders such as Alzheimer's disease and dietary restriction can enhance plasticity and decrease the rate of memory loss and enhance the capacity of stress response of the brain [ 17 ]. However, the benefits are noticed with adherence to quality diet; maximum improvement in cognitive decline with higher adherence to a more nutritious diet [ 18 ]. Neuroprotection: The prefrontal lobe is responsible for working memory [ 20 ].
Chapman et al. Executive function and temporal lobe are responsible for long term memory [ 22 ]. In the animal studies, the effects were seen at molecular levels such as neurogenesis, synaptogenesis, gliogenesis, and angiogenesis.
It occurred due to the increase expression of neurotransmitter and neurotrophin [ 23 ]. Lifestyle not only plays a role directly in neurogenesis but also stimulates microglia. The microglia protector of neuronal cells indirectly facilitates neurogenesis [ 7 ]. The experiment conducted in mouse conducted showed it is possible to delay the cognitive decline only if a healthier environment is maintained, such as physical activity and diet. If not maintained, then the benefits remain inconclusive [ 24 ].
They are likely to be increased during physical exercise. These cortices are most vulnerable to aging and also severely affected due to Alzheimer's disease AD [ 25 , 26 ].
Chronic stress can cause severe damage in the hippocampus, thus leading to a substantial decrement in neurogenesis. Hippocampal structural plasticity and neurogenesis can be modulated by hormones like sex, stress, and metabolic [ 28 ]. Physical exercise mostly increases the anterior part of the hippocampus that is responsible for spatial memory performance [ 29 ]. There is a tight relationship between the exercise and angiogenesis.
The blood volume increased with an increase in the intensity of the exercise by the process of angiogenesis the growth of new blood vessels [ 4 ]. The studies conducted in knocked out mice showed activation of the BDGF tyrosine kinase B TrkB pathways during chronic exercise and high interval intensity workout. This pathway is responsible for neuroprotection, neurogenesis, and neuroplasticity [ 30 ].
Our brain function and structure adapt according to the cognitive demand of exercise, which then prevents the brain from aging and age-related neurological disease [ 31 ]. As the intensity of PA increases, the expression of these chemicals increases. BDGF is responsible for hippocampal neurogenesis, dendritic complexity, and synaptic complexity and neuroplasticity [ 20 ].
BDGF concentration directly correlated with hippocampal volume [ 20 ]. Vascular endothelial growth factor VEGF is responsible for forming blood vessels in the brain, responsible for the process of neurogenesis. The study by Fabel et al. Inhibition of peripheral VEGF indicated that the exercise-induced neurogenesis was not present [ 32 ]. Orexin A and orexin B are neuropeptides synthesized from the lateral hypothalamus. They are accountable for regulating wakefulness and arousal, motivation and emotions, and motor and autonomic functions [ 33 , 34 ].
Healthy lifestyle adherence can build up brainpower and can lead to more prolonged survival, delayed aging, physical, and mental health [ 6 ]. When new neurons are integrated with existing circuits of new and old neurons, some of the old neurons get replaced. Thus, it shows blocking new synapse can prevent the removal of memories from the hippocampus. Mechanism of exercise-induced neurogenesis: Many researchers have discovered the significant effect of exercise-induced neurogenesis.
In one of the studies, male rats forced implementing a treadmill during their adolescence, demonstrated the decrease expression of BDGF throughout the brain. In contrast to this, the voluntary treadmill increases the expression of cannabinoid. It is responsible for hippocampal neurogenesis, especially the proliferation and migration of neurons in the dentate gyrus of the hippocampus [ 35 ]. During exercise, cathepsin B CTSB releases, and its expression gets enhanced, which results in enhancement of spatial memory, inhibitory transmission onto dentate gyrus of the hippocampus, and decreased hippocampus P11, a protein needed for CTSB effects on neuronal differentiation and migration.
A chronic behavior of physical activity up-regulates synaptic plasticity and neurogenesis that can be explained by the Wnt pathway. On the one-hand, adult rats who were on long-term exercise expressed a higher level of Wnt protein, on the other hand, rats those who had a sedentary lifestyle secreted more wnt antagonist, Dkk-1, the lowest level found in the exercised group [ 10 ].
Anti-apoptotic proteins such as Bcl-2 increased in mice who did exercise [ 10 ]. The elderly who did aerobic exercise responsible for up to 60 min can improve information processing, prevent atrophy of the hippocampus, and increase the neuronal volume of the hippocampus [ 21 ].
The most common behavioral changes in the elderly are cognitive loss and behavioral changes related to the atrophy of the brain.
They can be delayed by physical exercise, shown in a study performed in the white and black elder population [ 6 ]. In the population who completed a moderate amount of physical activity increased BDGF, synapsin facilitates neurotransmitter release; those who consume a high-fat diet have a low level of synapsin Exercise leads to the activation of various pathways mitogen-activated protein kinase MAPK such as increase protein transcription and eventually accelerates neurotransmitter release.
Hippocampal neurogenesis causes an increase in brain size and a decrease in apoptosis in the hippocampus to prevent in atrophy of the brain, therefore leading to significant prevention of spatial memory deficit in people who do exercise. One of the prime functions of exercise is to decrease pro-inflammatory cytokines, decrease insulin resistance, increase brain insulin signaling, principal to increase protein transcription, eventually expediting neurotransmitter release for spatial memory [ 37 ].
In one of the studies, adult hippocampus neurogenesis alone was not enough for improving cognition. Neurogenesis produced minimal benefit, as shown in mice.
Reduction of Ab load and increment of BDGF, interleukin-6, fibronectin type III domain-containing protein, and synaptic markers were equally significant along with exercise-induced neurogenesis [ 24 ]. Intrinsic hormones and extrinsic factors diet and exercise are responsible for neuroplasticity and neurogenesis. Based on an exercise regime, duration, and intensity can transform how neuronal plasticity can happen in the brain that can affect therapeutic approaches and help to regain the strength of an aging brain [ 5 ].
One of the forms of exercise is an acrobatic exercise that involves multiple muscle groups and produces a compound movement that can not only heightened neurogenesis but also promote learning. The study conducted in rats, which then evaluated includes the study of the cerebellum, the motor cortex, striatum, and hippocampus.
The result of this study concluded, exercise stimulates plasticity in brain areas of rats that are chiefly affected by the intensity and duration of the PA [ 28 ]. Daily sexual encounters for 14 consecutive days do not raise corticosterone levels, and actually decrease anxiety behavior while still promoting neurogenesis. Neurogenesis is higher in socialized rats compared to rats kept in isolation. Isolated rats show a significant reduction in BDNF in the hippocampus, and they also perform worse on memory tasks.
Social isolation also increases stress, and even cancels out the positive effects of running on neurogenesis. So if you live alone, be sure to make socializing part of your regular routine. There is a long list of foods that promote neurogenesis. Grapeseed extract, turmeric, green tea , and resveratrol found in peanuts, tree nuts, grapes, cocoa, wine, and berry fruits also promote the growth of new neurons. And fatty fish, seaweed, algae, walnuts, and flax, chia, and hemp seeds contain omega-3 polyunsaturated fatty acids PUFAs , which have been shown to promote hippocampal neurogenesis and improve spatial memory.
But the practice of intermittent fasting is a new trend due to research showing its benefits for a wide range of health conditions. As a result, intermittent fasting is built into our physiology, and research shows that it benefits our health in many ways. Intermittent fasting lowers our insulin level and blood pressure, reduces inflammation, helps clear out toxins and damaged cells, improves our stress resistance, lengthens our lifespan, and reduces incidence of diabetes, obesity, and cancer.
And of course, it increases neurogenesis and levels of BDNF , and prevents neuron death in the hippocampus. The simplest form of intermittent fasting limits all food intake to a certain window of time, like 6 hours a day. Researchers recommend the circadian rhythm fasting approach, in which you start eating in the morning and finish consuming all your food by mid-afternoon or early evening.
A study of men with prediabetes clearly showed the positive effects of early time-restricted feeding eTRF : lower insulin levels, improved insulin sensitivity, and lower blood pressure and oxidative stress. Surprisingly, the eTRF group also had less desire to eat in the evening. Eating a big meal in the evening is probably not good for our health, and researchers suggest that the ways our circadian rhythms affect our body temperature, biochemical reactions, hormone levels, physical activity, and digestion of food may be why.
Finally, you can stimulate neurogenesis with meditation. The cerebral cortex of people who practice meditation is thicker in the areas associated with attention, interoception internal sense of your body , and sensory processing. Differences in cortical thickness correlates with meditation experience, and meditation may offset age-related cortical thinning.
Experienced meditators also have larger hippocampi than non-meditators, and yoga and meditation increase levels of BDNF. We know that learning and repetition work. How do you know if something different represents a structural and functional change in your brain? When you make a lifestyle change—like getting more sleep, reducing alcohol intake, starting to meditate, or exercising more—notice the effects.
Do you feel happier or less stressed out? Are you able to focus better at work? And try envisioning the changes taking place in your brain. When you get faster at your computer game, visualize the neural circuits that control your play efficiently lighting up and sending their messages.
When you find yourself reacting less to potentially stressful events, imagine the calmness in your brain as it decides to not activate your stress response. We have just as much control over the health and function of our brains as we do our bodies.
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