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Memory improvement is the act of improving one's memory.
Medical research of memory deficits and age-related memory loss has resulted in new explanations and treatment techniques to improve memory, including diet, exercise, stress management, cognitive therapy and pharmaceutical medications. Neuroimaging as well as cognitive neuroscience have provided neurobiological evidence supporting holistic ways in which one can improve memory.
Memory function factorsEdit
Understanding that the human brain can change through experience is the first step to improving memory function. It was once thought that the adult brain was a fixed entity, however it has been found that the brain is actually a highly flexible and plastic organ that changes based upon our experiences, emotions and behavior. Neuroplasticity is the mechanism by which the brain encodes experience, learns new behaviours and relearns lost behaviour if the brain has been damaged.Experience-dependent neuroplasticity suggests that the brain changes in response to what it experiences. London taxicab drivers provide a great example of this dynamic. They undergo extensive training for 2–4 years, learning and memorizing street names, layout of streets within the city and the quickest cross-city routes. After studying London taxicab drivers over a period of time, it was found that the grey matter volume increased over time in the posterior hippocampus, an area in the brain involved heavily in memory. The longer taxi drivers navigated the streets of London, the greater the posterior hippocampal gray matter volume. This suggests a correlation between a healthy person's mental training or exercise and their brains capacity to manage greater volume and more complex information.
Rehabilitation research findingsEdit
Decades of neuroscience research of people with brain trauma or brain damage has resulted in the identification of 10 factors that may affect the outcome of their rehabilitation. They are also general guidelines to improve the memory of healthy individuals.
- Neural circuits not actively engaged in task performance for an extended period of time begin to degrade.
- Rehabilitative training, such as cognitive training.
- In many studies, learning or skill acquisition produced significant changes in patterns of neural connectivity over repetition of known behaviors.
- Repetition, though, may be required to induce long lasting neural changes. You are more likely to remember information with repetition because practice reduces the amount of effort the brain needs to expend when retrieving and processing information important for the task, allowing it to be faster and more automatic.
- The intensity of training stimulation can also affect the induction of neural plasticity. Low-intensity stimulation can induce a weakening of synaptic responses (long-term depression), whereas higher emotional intensity stimulation will induce long-term potentiation.
- In stimulation experiments, synaptic responses are more likely to degrade in early phases of stimulation rather than later and it has been proven that stable consolidation of memories requires time.
- The more important the information is, the greater the tendency to encode and recall the information. It has been shown that there is a tendency to orient attention towards stimuli that is salient. This allows for quick detection and reaction to objects in our environment.
- Aging results in a number of neuroplastic changes in the brain. Long-term potentiation (LTP), the increased transmission between two neurons, is said to be one of the underlying mechanisms of synaptic plasticity. Aging causes a reduction in LTP and therefore may cause a reduction in synaptic plasticity. Synaptogenesis, the formation of synapes, as well as cortical map reorganization are both also reduced with aging. Cognitive decline and age-related impairments may therefore reflect the progressive failure of plasticity processes. Although aging results in a decrease in plasticity, the aging brain is clearly responsive to experience and may change, even though the changes in the brain may be less profound and/or slower to occur than those observed in younger brains.
- Transference, the ability of plasticity within one set of neural circuits to promote concurrent or subsequent plasticity, can enhance the acquisition of similar behaviours.
- Interference, the ability of plasticity to impede new or existing plasticity within the same circuitry and potentially impair learning, can be disruptive to some learning and task performance.
Research has found that chronic and acute stress have adverse effects on memory processing systems. Therefore, it is important to find mechanisms in which one can reduce the amount of stress in their lives when seeking to improve memory.
- Chronic stress has been shown to have negative impacts on the brain, especially in memory processing systems. The hippocampus is vulnerable to repeated stress due to adrenal steroid stress hormones. Elevated glucocorticoids, a class of adrenal steroid hormones, results in increased cortisol, a well known stress response hormone in the brain, and glucocorticoids are known to affect memory. Prolonged high cortisol levels, as seen in chronic stress, have been shown to result in reduced hippocampal volume as well as deficits in hippocampal-dependent memory, as seen in impaired declarative, episodic, spatial, and contextual memory performance. Chronic, long-term high cortisol levels affect the degree of hippocampal atrophy, resulting in as much as a 14% hippocampal volume reduction and impaired hippocampus-dependent memory when compared to elderly subjects with decreased or moderate cortisol levels. An example may be found in the London taxi drivers, as the anterior hippocampus was hypothesized to decrease in volume as a result of elevated cortisol levels from stress.[nb 1]
- Acute stress, a more common form of stress, results in the release of adrenal steroids resulting in impaired short-term and working memory processes such as selective attention, memory consolidation, as well as long-term potentiation. The human brain has a limited short-term memory capacity to process information, which results in constant competition between stimuli to become processed. Cognitive control processes such as selective attention reduce this competition by prioritizing where attentional resources are distributed. Attention is crucial in memory processing and enhances encoding and strength of memory traces. It is therefore important to selectively attend to relevant information and ignore irrelevant information in order to have the greatest success at remembering.
- Animal and human studies provide evidence as they report that acute stress impairs the maintenance of short-term memory and working memory and aggravates neuropsychiatric disorders involved in short-term and working memory such as depression and schizophrenia. Animal studies with rats have also shown that exposure to acute stress reduces the survival of hippocampal neurons.
- One of the roles of the central nervous system (CNS) is to help adapt to stressful environments. It has been suggested that acute stress may have a protective function for individuals more vulnerable to their own stress hormones. Some individuals, for example, are not able to decrease or habituate their cortisol elevation, which plays a major role in hippocampal atrophy. This over-response of the central nervous system to stress therefore causes maladaptive chronic stress-like effects to memory processing systems.
Memory improvement strategiesEdit
Discovering that the brain can change as a result of experience has resulted in the development of cognitive training. Cognitive training improves cognitive functioning, which can increase working memory capacity and improve cognitive skills and functions in clinical populations with working memory deficiencies. Cognitive training may focus on attention, speed of processing, neurofeedback, dual-tasking and perceptual training.
Cognitive training has been shown to improve cognitive abilities for up to five years. In one experiment, the goal was to prove that cognitive training would increase the cognitive functions in older adults by using three types of training (memory, reasoning and speed of processing). It was found that improvements in cognitive ability not only was maintained over time but had a positive transfer effect on everyday functioning. Therefore, these results indicate that each type of cognitive training can produce immediate and lasting improvements in each kind of cognitive ability, thus suggesting that training can be beneficial to improving memory.
Cognitive training in areas other than memory has actually been seen to generalize and transfer to memory systems. For example, the Improvement in Memory with Plasticity-based Adaptive Cognitive Training (IMPACT) study by the American Geriatrics Society in 2009 demonstrated that cognitive training designed to improve accuracy and speed of the auditory system presented improvements in memory and attention system functioning as well as auditory functioning.
Two cognitive training methods are:
- Strategy training is used to help individuals remember increasing amounts of information of a particular type. It involves teaching effective approaches to encoding, maintenance, and/or recall from working memory. The main goal of strategy training is to increase performance in tasks requiring retention of information. Studies strongly support the claim that the amount of information remembered can be increased by rehearsing out loud, telling a story with stimuli, or using imagery to make stimuli stand out. Strategy training has been used in children with Down syndrome and also in older adult populations.
- Core training involves repetition of demanding working memory tasks. Some core training programs involve a combination of several tasks with widely varying stimulus types. The diversity of exercises increase the chance that one of, or some combination of the training tasks, will produce desired training-related gains. A goal of cognitive training is to impact the ease and success of cognitive performance in one’s daily life. Core training can reduce the symptoms of Attention deficit hyperactivity disorder (ADHD) and improve the quality of life involving patients with multiple sclerosis, schizophrenia and also, those who have suffered from stroke.
The manner in which a training study is conducted could affect the outcomes or perspection of the outcomes. Expectancy/effort effects occur when the experimenter subconsciously influences the participants to perform a desired result. One form of expectancy bias relates to placebo effects, which is the belief that training should have a positive influence on cognition. A control group may help to eliminate this bias because this group would not expect to benefit from the training. Researchers sometimes generalize their results, which can be misleading and incorrect. An example is to generalize findings of a single task and interpret the observed improvements as a broadly defined cognitive ability. The study may result in inconsistency if there are a variety of comparison groups used in working memory training, which is impacted by: training and assessment timeline, assessment conditions, training setting and control group selection.
- Epinephrine, also known as adrenaline, has been associated with memory enhancement in both humans and animals. Current evidence suggests memory consolidation in particular, appears to be enhanced by the administration of epinephrine. However, epinephrine also interacts with the level of arousal at the time of memory encoding and has resulted in improvement of low arousing object recognition in rats.
- Acetylcholine is an essential neurotransmitter in the brain, possibly regulated by glucose levels, which can improve working memory when at increased level in synapses. These findings are attributed to the important role played by acetylcholine in the maintenance of selective attention. Other studies have shown that rats with elevated neocortical acetylcholine levels have significantly improved performance on spatial navigation tasks. Furthermore, acetylcholine is not only necessary for memory but its presence has been found to restore spatial memory in rats with damage to the nucleus basalis. Evidence that aspects of memory can be improved by action on selective neurotransmitter systems, such as the cholinergic system which releases acetylcholine, has possible therapeutic benefits for patients with cognitive disorders.
- Nicotine. Findings from both human and animal studies have indicated that acute administration of nicotine can improve cognitive performance (particularly tasks that require attention), short-term episodic memory and prospective memory task performance. Chronic usage of low-dose nicotine in animals has been found to increase the number of neuronal nicotinic acetylcholine receptors (nAChRs) and improve performance on learning and memory tasks. Short-term nicotine treatment, utilising nicotine skin patches, have shown that it may be possible to improve cognitive performance in a variety of groups such as normal non-smoking adults, Alzheimer’s disease patients, schizophrenics, and adults with attention-deficit hyperactivity disorder. Similarly, evidence suggests that smoking improves visuospatial working memory impairments in schizophrenic patients, possible explaining the high rate of tobacco smoking found in people with schizophrenia. However, evidence suggests that low doses of nicotine facilitate memory and high doses have no significant effect or may impair memory.
Research suggests that what food we eat can influence memory processing. Glucose, flavanoids, fat and calories all affect memory areas of the brain.
- Flavonoids are photochemicals mainly found in plant-based foods known for their antioxidant activity and are found to improve memory.
- The main dietary groups of flavonoids are:
- flavonols, found in onions, leeks and broccoli
- flavones, found in parsley and celery
- isoflavones, found in soybean and soya products
- flavanones, found in citrus fruit and tomatoes
- flavanols, which are abundant in green tea, red wine and cocoa
- anthocyanidins, whose sources include red wine and berry fruits.
- Human and animal research using flavonoids such as grapes, tea, cocoa, blueberries, as well as ginkgo biloba extracts, have all shown beneficial effects on mental performance. Flavonoids interact with brain-derived neurotrophic factor (BDNF), a neurotrphin important to long-term potentiation (LTP), to improve human memory by enhancing neuronal function, stimulating neuronal regeneration (neurogenesis) and protecting existing neurons against oxidative and metabolic stress. They also interact with a signalling pathway increasing neurotrophin proteins, synaptic strength between neurons and synaptic plasticity. Human brain-imaging studies demonstrate that when consuming flavanol-rich cocoa, there is an increase in cortical blood flow, important to the hippocampus for facilitation of neurogenesis. Flavonoids are suggested to be used as a dietary intervention to improve memory as they are able to enhance neuronal function, stimulate neuronal regeneration and protect existing neurons.
- Glucose. Research has suggested that glucose, a major source of energy used by the central nervous system and transported from blood to brain for cognitive functions, may enhance memory processing by altering neural metabolism and neurotransmitter synthesis in the brain. Glucose influences the synthesis of hippocampal acetylcholine (ACh), an essential neurotransmitter in the brain.
- As a person ages, their body's ability to utilize glucose decreases. Studies on glucose and memory have indicated that moderate increases in glucose levels may enhance memory formation in both animals and humans and may play a major role in memory deficits found in aging, healthy young subjects, and people with Alzheimer's disease and Down syndrome. A dose-response relationship for glucose effects on memory was found to represent an inverted-U, in which moderate doses enhance memory while higher doses impair it. Eating meals more frequently during the day can aid in maintaining moderate blood glucose levels, which provides the brain with a consistent source of high energy.
- Fats. Animal studies have shown that diets rich in saturated fats, hydrogenated fats and or cholesterol can impair cognitive performance, memory and hippocampal morphology. These rats produced more errors in working memory maze tasks and indicated a loss of dendritic integrity in the hippocampus as seen from reduced hippocampal staining and inflammation. Human studies on Alzheimer's disease (AD) can be used to suggest that saturated fats, cholesterol, high calorie diets that are vitamin and antioxidant deficient promote the onset of the Alzheimer's disease whereas diets high in mono- and polyunsaturated fatty acids as well as omega-3 fatty acids however may decrease the risk of AD. Individuals with high cholesterol diets have also been seen to increase risk of AD, while those taking cholesterol-lowering drugs may have a decreased risk.
- Calories. High calorie diets have been found to increase the risk of Alzheimer's disease; Caloric restriction can improve memory by providing a protective function which reduces the amount of neuronal dysfunction and degeneration. Moving away from a high calorie diet can improve memory by producing brain-derived neurotrophic factor (BDNF) that enhances memory through synaptic growth and protection.
Data from studies suggests that diets low in saturated fat, cholesterol and calories may reduce the risk of Alzheimer's disease (AD), may aid in protecting and improving memory.
Meditation, a form of mental training to focus attention, has been shown to increase the control over brain resource distribution, improving both attention and self-regulation. The changes are potentially long-lasting as meditation may have the ability to strengthen neuronal circuits as selective attentional processes improve. Meditation may also enhance cognitive limited capacity, affecting the way in which stimuli are processed.
Studies have found that meditation significantly decreases stress related cortisol secretion and may elevate brain-derived neurotrophic factor, which protects neurons against stress and stimulates the production of new neurons. Meditation practice has also been associated with physical changes in brain structure. Magnetic resonance imaging (MRI) of Buddhist insight meditation practitioners who practiced mindfulness meditation were found to have an increase in cortical thickness and hippocampus volume compared to the control group. This research provides structural evidence that meditation practice promotes neural plasticity and experience-dependent cortical plasticity.
In both human and animal studies, exercise has been shown to improve cognitive performance on encoding and retrieval tasks. Morris water maze and radial arm water maze studies of rodents found that, when compared to sedentary animals, exercised mice showed improved performance traversing the water maze and displayed enhanced memory for the location of an escape platform. Likewise, human studies have shown that cognitive performance is improved due to physiological arousal, which speeded mental processes and enhanced memory storage and retrieval. Ongoing exercise interventions have been found to favourably impact memory processes in older adults and children.
Exercise has been found to positively regulate hippocampal neurogenesis, which is considered an explanation for the positive influence of physical activities on memory performance. Hippocampus-dependent learning, for example, can promote the survival of newborn neurons which may serve as a foundation for the formation of new memories. Exercise has been found to increase the level of brain-derived neurotrophic factor (BDNF) protein in rats, with elevated BDNF levels corresponding with strengthened performance on memory tasks. Data also suggests that BDNF availability at the beginning of cognitive testing is related to the overall acquisition of a new cognitive task and may be important in determining the strength of recall in memory tasks.
Evidence suggests that administering oxygen enhances memory function. For example, adult participants who inhaled oxygen sixty seconds before the presentation of a word list that was to be studied, showed improved recall compared to a group who did not. Blood oxygen saturation and heart rate are positively correlated with each other. Research has found that an increased heart rate during word recall is associated with improved memory performance.
Administering oxygen before the test, though, had no effect, suggesting that increased blood oxygen saturation specifically enhances memory consolidation.
Aristotle wrote a treatise about memory: De memoria et reminiscentia. To improve recollection, he advised that a systematic search should be made and that practice was helpful. He suggested grouping the items to be remembered in threes and then concentrating upon the central member of each triad (group of three).
Music playing has recently gained attention as a possible way to promote brain plasticity. Promising results have been found suggesting that learning music can improve various aspects of memory. For instance, children who participated in one year of instrumental musical training showed improved verbal memory, whereas no such improvement was shown in children who discontinued musical training. Similarly, adults with no previous musical training who participated in individualized piano instruction showed significantly improved performance on tasks designed to test attention and working memory compared to a healthy control group. Evidence suggests that the improvements to verbal, working and long-term memory associated to musical training are a result of the enhanced verbal rehearsal mechanisms musicians possess.
- Music-related memory
- Sleep and Memory
- Effect of caffeine on memory
- Cognitive enhancer
- Working memory training
- Emotion and memory
- ↑ Quote from Maguire: "Increases in plasma or salivary cortisol are often used as a biochemical marker of stress. Elevated cortisol levels have been associated with poor performance on memory tasks (Newcomer et al., 1999; Cho et al., 2000) and reduced hippocampal volume (Lupien et al., 1998). Thus, stress may have induced the anterior hippocampal volume reduction in the taxi drivers."
- ↑ 1.0 1.1 Brown, J. and Fenske, M. (2010). The Winners Brain. De Capo Press: United States of America. Pages 219-161.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Kleim, JA., & Jones, TA. (2008). Principles of experience-dependent neural plasticity: implications for rehabilitation after brain damage. Journal of Speech, Language, and Hearing Research, 51, S225-S239.
- ↑ 3.0 3.1 3.2 Maguire, EA., Woollett, K., & Spiers, HJ. (2006). London taxi drivers and bus drivers: a structural MRI and neuropsychological analysis. Hippocampus, 16, 1091-1101.
- ↑ Fine, M.S., Minnery, B.S. (2009).Visual Salience Affects Performance in a Working Memory Task. The Journal of Neuroscience. Vol 29(25): 8016-8021.
- ↑ 5.0 5.1 Cooke SF, Bliss TV (2006). "Plasticity in the human central nervous system". Brain 129 (Pt 7): 1659–73.
- ↑ 6.0 6.1 6.2 6.3 Mizoguchi, K., Mitsutoshi, Y., Ishige, A., et al. (2000). Chronic Stress Induces Impairment of Spatial Working Memory Because of Prefrontal Dopaminergic Dysfunction. The Journal of Neuroscience Vol 20(4) 1568-1574.
- ↑ Jacobson, L. & Sapolsky, R.M.The role of the hippocampus in feedback regulation of the hypothalamic-pituitary-adrenal axis. Endo. Rev. 12, 118−134 (1991).
- ↑ Starkman, M. N., Gebarski, S. S., Berent, S. & Schteingart, D. E.(1992). Hippocampal formation volume, memory dysfunction, and cortisol levels in patients with Cushing's syndrome. Biol. Psychiatry 32, 756−765.
- ↑ 9.0 9.1 9.2 McEwen, B.S. (1999). Stress and Hippocampal Plasticity. Annual Review of Neuroscience. Vol. 22: 105-122.
- ↑ Squire, L. R.(1992). Memory and the hippocampus : A synthesis from findings with rats, monkeys, and humans. Psychol. Rev. 99, 195−231.
- ↑ Sapolsky, R. M., Krey, L. C. & McEwen, B. S. (2002) The neuroendocrinology of stress and aging: The glucocorticoid cascade hypothesis. Endo. Rev. 7, 284−301.
- ↑ Lupien SJ, McEwen BS. 1997. The acute effects of corticosteroids on cognition: integration of animal and human model studies. Brain Res. Rev. 24:1–27.
- ↑ McEwen, B.S. (1998). Protective and damaging effects of stress mediators. New Engl. J. Med. 238, 171−179.
- ↑ Shiffrin, R.M. (1976). Capacity limitations in information processing, attention, and memory. In W.K. Estes (Ed.), Handbook of learning and cognitive processes (Vol. 4). Hillsdale, NJ: Erlbaum.
- ↑ 15.0 15.1 15.2 Slagter, H.A., Lutz, A., Greischar, L.L., Francis, A.D., Nieuwenhuis, S., Davis, J.M., Davidson, R.J. (2007). Mental Training Affects Distribution of Limited Brain Resources. PLoS Biol Vol 5(6).
- ↑ 16.0 16.1 16.2 Tang, Y.Y., Ma, Y. Wang, Y., Fan, Y. Et al. (2007). Short-term meditation training improves attention and self-regulation.PNAS. vol. 104 no. 43 17152-17156.
- ↑ Kirschbaum C, Prussner JC, Stone AA, Federenko I, Gaab J. 1995. Persistent high cortisol responses to repeated psychological stress in a subpopulation of healthy men. Psychosomat. Med. 57:468–74.
- ↑ 18.0 18.1 18.2 18.3 18.4 Morrison, AB., & Chein, JM. (2010). Does working memory training work? the promise and challenges of enhancing cognition by training working memory. Psychonomic Society, Inc.
- ↑ Willis, SL., Tennstedt, SL., Marsiske, M., Ball, K., Elias, J., Koepke, KM., Morris, JN., Rebok, GW., Unverzagt, FW., Stoddard, AM., & Wright, E. (2006). Long-term effects of cognitive training on everyday functional outcomes in older adults. National Institutes of Health, 296(23), 2805-2814.
- ↑ Smith, G.E., Housen, P., Yaffe , K., Ruff, R., Kennison, R.F., Mahncke , H.W., Zelinski, E.M. (2009). A Cognitive Training Program Based on Principles of Brain Plasticity: Results from the Improvement in Memory with Plasticity-based Adaptive Cognitive Training (IMPACT) Study. The American Geriatrics Society.
- ↑ Cahill, L., & Alkire, M. T. (2003). Epinephrine enhancement of human memory consolidation: Interaction with arousal at encoding. Neurobiology of Learning and Memory, 79, 194–198.
- ↑ Flint, R. W., Bunsey, M. D., & Riccio D. C. (2007). Epinephrine-induced enhancement of memory retrieval for inhibitory avoidance conditioning in preweanling sprague–dawley Rats. Dev Psychobiol, 49, 303–311.
- ↑ Jurado-Berbel, P., Costa-Miserachs, D., Torras-Garcia, M., Coll-Andreu, M., & Portell-Cortés, I. (2010). Standard object recognition memory and “what” and “where” components: Improvement by post-training epinephrine in highly habituated rats. Behavioural Brain Research, 207, 44–50.
- ↑ Furey, M. L., Pietrini, P., Haxby, J. V. & Drevets, W. C. (2008). Selective effects of cholinergic modulation on task performance during selective attention. Neuropsychopharmacology, 33, 913–923.
- ↑ Winkler, J., Suhr, S. T., Gage, F. H., Thal, L. J., & Fisher, L. J. (1995). Essential role of neocortical acetylcholine in spatial memory. Nature, 375, 484 – 487.
- ↑ Robbins, T. W., Mehta, M. A., & Sahakian, B. J. (2000). Boosting working memory. Science, 20, 2275–2276.
- ↑ 27.0 27.1 Üzum, G., Diler, A. S., Bagcekapili, N., Tasyurekli, M. T., & Ziylan, Y. Z. (2004). Nicotine improves learning and memory in rats: morphological evidence for acetylcholine involvement. Intern. J. Neuroscience, 114:1163-1179.
- ↑ Heishman, S. J., Kleykamp, B. A., & Singleton, E. G. (2010). Meta-analysis of the acute effects of nicotine and smoking on human performance. Psychopharmacology, 210:453–469.
- ↑ Jennifer M Rusted, J. M., & Trawley, S. (2006). Comparable Effects of Nicotine in Smokers and Nonsmokers on a Prospective Memory Task. Neuropsychopharmacology, 31, 1545–1549.
- ↑ Swan, G. E., & Lessov-Schlaggar, C. N. (2007). The effects of tobacco smoke and nicotine on cognition and the brain. Neuropsychol Rev, 17:259–273.
- ↑ Sacco, K. A., Termine, A., Seyal, A., Dudas, M. M., Vessicchio, J. C., Krishnan-Sarin, S., Jatlow, P. I., Bruce E. Wexler, B. E., & George, T. P. (2005). Effects of cigarette smoking on spatial sorking memory and attentional deficits in schizophrenia. ARCH GEN PSYCHIATRY, 62, 659—659.
- ↑ 32.0 32.1 Manach C, Scalbert A, Morand C, Remesy C & Jimenez L (2004) Polyphenols: food sources and bioavailability. American Journal Clinical Nutrition 79, 727–747.
- ↑ Youdim KA, Spencer JPE, Schroeter H & Rice-Evans C (2002) Dietary flavonoids as potential neuroprotectants. BiolChem 383, 503–519.
- ↑ 34.0 34.1 34.2 Spencer, J.P.E. (2008). Food for thought: the role of dietary flavonoids in enhancing human memory, learning and neuro-cognitive performance. Proceedings of the Nutrition Society. Vol 67, 238–252.
- ↑ 35.0 35.1 35.2 Lee J, Seroogy KB, Mattson MP. Dietary restriction enhances neurotrophin expression and neurogenesis in the hippocampus of adult mice. J Neurochem. 2002; 80:539-47.
- ↑ Yamada K, Nabeshima T (April 2003). "Brain-derived neurotrophic factor/TrkB signaling in memory processes". J. Pharmacol. Sci. 91 (4): 267–70.
- ↑ Reichardt LF (September 2006). "Neurotrophin-regulated signalling pathways". Philos. Trans. R. Soc. Lond., B, Biol. Sci. 361 (1473): 1545–64.
- ↑ Schroeter H, Heiss C, Balzer J, Kleinbongard P, Keen CL, Hollenberg NK, Sies H, Kwik-Uribe C, Schmitz HH & Kelm M (2006) (-)-Epicatechin mediates beneficial effects of flavanol-rich cocoa on vascular function in humans. Proc Natl Acad Sci USA 103, 1024–1029.
- ↑ 39.0 39.1 Ragozzino, M.E., Unick, K.E., Gold, P.E. (1996). Hippocampal acetylcholine release during memory testing in rats: augmentation by glucose. PNAS. vol. 93 no. 10 4693-4698.
- ↑ 40.0 40.1 Korol, D.L. & Gold, P.E. (1998). Glucose, memory, and aging. American Journal of Clinical Nutrition Vol. 67.
- ↑ 41.0 41.1 41.2 Hall, J. L., Gonder-Frederick, L. A., Chewning, W. W., et al. (1989). Glucose Enhancement of Performance on Memory Tests in Young and Aged Humans. Neuropsychologia Vol. 21. No. 9, pp 1129-l 138.
- ↑ Granholm . A.C., Bimonte-Nelson . H.A., Moore , A.B., et al. (2008). Effects of a Saturated Fat and High Cholesterol Diet on Memory and Hippocampal Morphology in the Middle-Aged Rat. Journal of Alzheimer's Disease. Vol.14(2).
- ↑ Ramesh, B.N., Sathyanarayana Rao, T.S., Prakasam, A., Sambamurti, K., et al. (2010). Neuronutrition and Alzheimer's Disease. Journal of Alzheimer's Disease. Vol 19(4).
- ↑ Kalmijn, S. (2000). Fatty acid intake and the risk of dementia and cognitive decline: a review of clinical and epidemiological studies. J. Nutr. Health Aging 4, 202−207
- ↑ Puglielli, L., Tanzi, R. E. & Kovacs, D. M. (2003). Alzheimer's disease: the cholesterol connection. Nature Neurosci. 6, 345−351
- ↑ Mattson MP, ed. Diet-Brain Connections: Impact on Memory, Mood, Aging and Disease. Boston: Kluwer; 2002.
- ↑ 47.0 47.1 Xiong, G.L. and Doraiswamy, M. (2009). "Does Meditation Enhance Cognition and Brain Plasticity?" Annals of the New York Academy of Sciences. Vol 1172, pages 63-69.
- ↑ Luders , E., Toga, A.W., Lepore , N., Gaser, C. (2009). The underlying anatomical correlates of long-term meditation: Larger hippocampal and frontal volumes of gray matter. NeuroImage Volume 45, Issue 3. Pages 672-678.
- ↑ Lazar, S.W., Kerr, C.E., Wasserman, R.H., et al. (2005). Meditation experience is associated with increased cortical thickness. Neuroreport. Vol 16(17) 1893–1897.
- ↑ 50.0 50.1 Berchtold, N. C., Castello, N., & Cotman, C. W. (2010). Exercise and time-dependent benefits to learning and memory. Neuroscience 167, 588–597.
- ↑ Lambourne, K., & Tomporowski, P. (2010). The effect of exercise-induced arousal on cognitive task performance: A meta-regression analysis. Brainresearch, 1341, 1 2 – 2 4.
- ↑ Colcombe, S. J., Kramer, A. F. (2003). Fitness effects on the cognitive function of older adults: a meta-analytic study. Psychol. Sci. 14, 125–130.
- ↑ Hillman, C .H., Castelli, D. M., Buck, S. M. (2005). Aerobic fitness and neurocognitive function in healthy preadolescent children. Med. Sci. Sports Exerc. 37, 1967–1974.
- ↑ van Praag H, Kempermann G, Gage FH. 1999b. Running increases cell proliferation and neurogenesis in the adult mouse dentate gyrus. Nat Neurosci 2:266–270.
- ↑ Van der Borght, K., Havekes, R., Bos, T., Eggen, B. J., & Van der Zee, E. A. (2007). Exercise Improves Memory Acquisition and Retrieval in the Y-Maze Task: Relationship With Hippocampal Neurogenesis. Behavioral Neuroscience, 121 (2), 324–334.
- ↑ 56.0 56.1 Moss, M. C., & Scholey, A. B. (1996). Oxygen administration enhances memory formation in healthy young adults. Psychopharmacology, 124, 255-260.
- ↑ Chung, S. C., & Lim, D. W. (2008). Changes in memory performance, heart rate and blood oxygen saturation due to 30% oxygen administration. International Journal of Neuroscience, 114:593–606.
- ↑ Anne Whitehead, "Memory and Inscription", Memory, pp. 15–49
- ↑ Wan, C. Y., & Schlaug, G. (2010). Music making as a tool for promoting brain plasticity across the life span. The Neuroscientist, 16(5), 566– 577.
- ↑ Bugos, J. A., Perlstein, W. M., McCrae, C. S., Brophy, T. S., & Bedenbaugh, P. H. (2007). Individualized Piano Instruction enhances executive functioning and working memory in older adults. Aging & Mental Health, 11(4): 464–471.
- ↑ Franklin, M. S., Moore, K., Yip, C., Jonides, J., Rattray, K., & Moher, J. (2008). The effects of musical training on verbal memory. Psychology of Music, 36(3), 353 – 365.
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