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Healthy Brain and Well-being: Sedentary lifestyle can impact cognitive ability adversely
Abstract
A sedentary lifestyle is one of the risk factors for a wide range of neurological and psychiatric diseases. Molecular and biochemical evidences support that sedentary lifestyle, excessive calorie intake and obesity can lead to a progressive decline in cognitive function. Studies on rodent models suggest that aerobic training can enhance cognitive skills irrespective of age. It improves blood flow in the brain, encourages the formation of new neurons and increases the number of synaptic connections between the neurons. Exercise prevents memory loss by reducing feelings of stress, anxiety and depression. Most of the results interlinking physical inactivity to loss in cognition are from studies on cerebral cortex and hippocampus, regions that are known for learning and memory. Further, exercise when initiated in the sedentary may result in adaptive cellular responses and up-regulation of genes responsible for neurogenesis in these regions. A few examples have been discussed on the brain from sedentary animals and humans, and the influence of exercise in protecting from accelerated loss in cognitive function in the physically inactive subjects.
... Similar to TLE, dementia/Alzheimer's disease (AD) pathology also share impairments in brain networks associated with hippocampus, and hence have similar behavioural and cognitive disturbances (Asha Devi et al., 2011;Saura et al., 2004). In AD, accumulation of Aβ peptides in hippocampus leads to degeneration of synapses, circuit reorganization and aberrant synchronization of networks, which are also involved in seizure generation and memory impairment in TLE (Jeffry, 2011;Saura et al., 2004). ...
Epilepsy is a neurological condition associated with seizures, neurodegeneration, circuit reorganization, and other structural and functional abnormalities. These elements ultimately lead to behavioural alterations such as anxiety, depression, and importantly cognitive impairment like learning disability and memory impairment. These factors can attribute to acceleration of aging and cognitive impairment in middle-aged people, which is otherwise evident in dementia and Alzheimer's disease among elderly people. In addition to epilepsy per se, several studies have shown that conventional anti-epileptic drugs used to treat epilepsy also contributes to aging and cognitive deficits through their adverse effects. The current review focuses on prevention of accelerated aging and cognitive impairment through an unconventional approach of combining non-pharmacological (enriched environment) and pharmacological therapy, which reduces the factors responsible for accentuated aging and memory impairment in chronic epileptic condition.
Polygonum is an important genus of Polygonaceae and Polygonum posumbu is underutilized traditional medicinal plant whose leaves are extensively used as an antipyretic and dyspepsia agent in Manipur, India as well as a spice in India, Japan, Nepal, China, South Korea, Philippines and Thailand. P. posumbu is commonly known as Phak-pai in Manipur. DNA barcode based molecular characterization technology for species identification has been recognized as a reliable tool for plants but the selection of suitable universal marker is still under discussion. The main aim of the study is to identify the Polygonum posumbu sample from Manipur, India using DNA barcode method. In the present study, Polygonum posumbu samples were collected from a local farmer in Awang khunou, Imphal West, Manipur, India which was taxonomically identified. To assess the molecular species identification, Internal Transcribed spacer (ITS) marker system was employed and the primer’s pair used were covered the internal transcribed spacer 1, 5.8S ribosomal RNA gene and internal transcribed spacer 2 complete sequence. Phylogenetic tree was constructed for the studied sample with the sequences of the 9 species retrieved from the GenBank in order to show the relationships among the samples. The result shows that the ITS marker-based DNA identification method successfully characterized the Polygonum posumbu species. The information of ITS marker-based identification of Polygonum posumbu from Manipur, India, will enhance our knowledge in better understanding the medicinal properties of this plant.
It has been widely accepted in the literature that various forms of physical exercise, even in a single session, enhance positive mood. It has also been shown that physical exercise may sometimes enhance creative thinking, but the evidence is inconclusive. Positive moods can favour creative thinking, but the opposite has also been reported and these relations are unclear. There is a large anecdotal literature suggesting that creative people sometimes use bodily movement to help overcome "blocks". The aim of this study was to establish whether post-exercise creative thinking was attributable to improved mood.
The responses of 63 participants to an exercise (aerobic workout or aerobic dance) and a "neutral" video watching condition were compared. Mood was measured using an adjective list, and creative thinking was tested by three measures of the Torrance test.
Analysis of variance showed a large and significant increase in positive mood after exercise (P < 0.001) and a significant decrease in positive mood after video watching (P < 0.001). A significant increase between the creative thinking scores of the two conditions was found on the flexibility (variety of responses) measure (P < 0.05). A multifactorial analysis of all data failed to show a significant covariance of creative thinking with the two measures of mood (P > 0.05).
These results suggest that mood and creativity were improved by physical exercise independently of each other.
Self-stimulation (SS) rewarding experience induced structural changes have been demonstrated in the hippocampal and motor cortical pyramidal neurons. In the present study, we have evaluated whether these changes are accompanied by neurochemical alterations in the hippocampus and motor cortex in SS experienced rats. Self-stimulation experience was provided one hour daily over a period of 10 days through stereotaxically implanted bipolar stainless steel electrodes, bilaterally in lateral hypothalamus and substantia nigra-ventral tegmental area. Self-stimulation experience resulted in a significant (P < 0.001) increase in the levels of noradrenaline, dopamine, glutamate and AChE activity but not 5-hydroxytryptamine and GABA levels in hippocampus and motor cortex. Such alterations in the levels of neurotransmitters may enhance the cognitive functions in the SS experienced rats.
Inspite of large number of studies on the neurochemical changes in the stress, an equivocal case is yet to be made for the role of a specific neurotransmitter in this important neurobiological disorder. The difficulty arises from the fact that there is no single neurotransmitter system appears to be responsible for the stress induced damage to the hippocampal neurons. The present study evaluates the effect of restraint stress on the alterations in the levels of biogenic amines, aminoacids and acetylcholinesterase activity in the hippocampus. Male Wistar rats of 45 days old were subjected to 6 hours of daily restraint stress over a period of 21 days. Immediately after the last session of stress, rats were sacrificed and neurotransmitter levels were estimated in the hippocampus. A significant (p < 0.001) decrease in the levels of noradrenaline, dopamine, 5-hydroxytryptamine and acetylcholinesterase activity in the stressed rats was observed compared to controls. However, levels of glutamate was significantly (p < 0.001) increased in stressed rats. These results indicate that chronic restraint stress decreases aminergic and cholinergic neurotransmission, and increases the glutamatergic transmission in the hippocampus.
Nitric oxide (NO) is a multifunctional molecule synthesized by three isozymes of the NO synthase (NOSs) acting as a messenger/modulator and/or a potential neurotoxin. In rodents, the role of NOSs in sleep processes and throughout aging is now well established. For example, sleep parameters are highly deteriorated in senescence accelerated-prone 8 (SAMP8) mice, a useful animal model to study aging or age-associated disorders, while the inducible form of NOS (iNOS) is down-regulated within the cortex and the sleep-structures of the brainstem. Evidence is now increasing for a role of iNOS and resulting oxidative stress but not for the constitutive expressed isozyme (nNOS). To better understand the role of nNOS in the behavioural impairments observed in SAMP8 versus SAMR1 (control) animals, we evaluated age-related variations occurring in the nNOS expression and activity and nitrites/nitrates (NOx-) levels, in three brain areas (n = 7 animals in each group). Calibrated reverse transcriptase (RT) and real-time polymerase chain reaction (PCR) and biochemical procedures were used.
We found that the levels of nNOS mRNA decreased in the cortex and the hippocampus of 8- vs 2-month-old animals followed by an increase in 12-vs 8-month-old animals in both strains. In the brainstem, levels of nNOS mRNA decreased in an age-dependent manner in SAMP8, but not in SAMR1. Regional age-related changes were also observed in nNOS activity. Moreover, nNOS activity in hippocampus was found lower in 8-month-old SAMP8 than in SAMR1, while in the cortex and the brainstem, nNOS activities increased at 8 months and afterward decreased with age in SAMP8 and SAMR1. NOx- levels showed profiles similar to nNOS activities in the cortex and the brainstem but were undetectable in the hippocampus of SAMP8 and SAMR1. Finally, NOx- levels were higher in the cortex of 8 month-old SAMP8 than in age-matched SAMR1.
Concomitant variations occurring in NO levels derived from nNOS and iNOS at an early age constitute a major factor of risk for sleep and/or memory impairments in SAMP8.
A sound mind resides in a sound body. Many individuals with an active lifestyle show sharp mental skills at an advanced age. Regular exercise has been shown to exert numerous beneficial effects on brawn as well as brain. The present study was undertaken to evaluate the influence of swimming on memory of rodents. A specially designed hexagonal water maze was used for the swimming exposures of animals. The learning and memory parameters were measured using exteroceptive behavioral models such as Elevated plus-maze, Hebb-Williams maze and Passive avoidance apparatus. The rodents (rats and mice) were divided into twelve groups. The swimming exposure to the rodents was for 10- minute period during each session and there were two swimming exposures on each day. Rats and mice were subjected to swimming for -15 and -30 consecutive days. Control group animals were not subjected to swimming during above period. The learning index and memory score of all the animals was recorded on 1(st), 2(nd), 15(th), 16(th), 30(th) and 31(st) day employing above exteroceptive models. It was observed that rodents that underwent swimming regularly for 30- days showed sharp memories, when tested on above behavioral models whereas, control group animals showed decline in memory scores. Those animals, which underwent swimming for 15- days only showed good memory on 16(th) day, which however, declined after 30-days. These results emphasize the role of regular physical exercise particularly swimming in the maintenance and promotion of brain functions. The underlying physiological mechanism for improvement of memory appears to be the result of enhanced neurogenesis. Key PointsMaintaining brain health throughout life is an important public health goal.Our results point out that integration of exercise schedule into the life style of Alzheimer patients is advantageous and worthwhile.Exercising regularly as you get older may not only keep your body in shape, but your brains as well.
We have shown previously that chronic restraint stress causes atrophy of apical dendrites and alter a- tions in the spine density of CA3 hippocampal neurons in rats. In the present study, the effect of 45 days of rehabilitation following 21 days of restraint stress on the dendritic morphology of CA3 neurons of the hippocampus was carried out. The results revealed that 45 days of rehabilitation reverses restraint stress-induced (6 h/day for 21 days) apical dend- ritic atrophy in CA3 neurons of the hippocampus. Whereas prolonged repeated restraint stress during this period also resulted in an atrophy of basal dendrites, suggesting that long-term stress can affect the hippocampal neurons more severely. These results showed that chronic stress-induced structural patho- logy of hippocampal neurons can be completely reversed by rehabilitation.
The effect of vitamin E on the accumulation of lipofuscin-containing fluorescent material in the mouse cerebral cortical cells in primary culture was studied. Fluorescent material was extracted in ethanol:diethylether (3:1) and autofluorescence intensity of the extracts was measured by a spectrofluorophotometer. Although vitamin E at the concentration of 0.005 IU/ml was not effective, 0.01 IU/ml vitamin E inhibited the accumulation of fluorescent material. Fluorescent material accumulation was reduced to 76.3-86.4% of the control level in 6-, 12-, or 18-day treatment of 0.01 IU/ml vitamin E. High doses of vitamin E (0.05 or 0.1 IU/ml) were toxic for cultured cells. Ethanol, the vehicle of vitamin E, at the final concentration of 0.005% was also effective on the reduction of fluorescent material accumulation (81.0% of the control level at 18 days). The inhibitory effects of vitamin E as well as ethanol on the accumulation of fluorescent material in cultured cells are explained by their nature as free radical scavengers.
The purpose of this study was to determine the psychological, behavioral, and cognitive changes associated with up to 14 months of aerobic exercise training. For the first 4 months of the study, 101 older (greater than 60 years) men and women were randomly assigned to one of three conditions: Aerobic exercise, Yoga, or a Waiting List control group. Before and following the intervention, all subjects completed a comprehensive assessment battery, including measures of mood and cognitive functioning. A semi-crossover design was employed such that, following completion of the second assessment, all subjects completed 4 months of aerobic exercise and underwent a third assessment. Subjects were given the option of participating in 6 additional months of supervised aerobic exercise (14 months total), and all subjects, regardless of their exercise status, completed a fourth assessment. Results indicated that subjects experienced a 10-15% improvement in aerobic capacity. In general, there were relatively few improvements in cognitive performance associated with aerobic exercise, although subjects who maintained their exercise participation for 14 months experienced improvements in some psychiatric symptoms. However, the healthy subjects in this study were functioning at a relatively high level to begin with, and exercise training may produce greater improvements among elderly with concomitant physical or emotional impairments.
Laboratory studies indicate that the life-span of inbred rodent strains is inversely related to the intensity of their behavioral and neuroendocrine responses to stressful stimuli. In the brain, a shorter life-span is associated with accelerated age-dependent degenerative changes in specific stress-responsive neuronal systems. The evidence suggests a possible genetic linkage between the intensity of the stress response, the rate of age-dependent neurodegeneration and the individual's life expectancy. It is proposed that inherent hyper-reactivity to stressors is genetically linked to a shorter life-span and to accelerated age-dependent neurodegeneration. Several experimental approaches to test 'this stress-longevity-neurodegeneration linkage hypothesis' are outlined.
Self-stimulation rewarding experience promoted structural changes in pyramidal neurons of the CA3 region of the hippocampus and the Vth layer of the motor cortex in adult male Wistar rats. Self-stimulation experience was allowed for 1 h daily for a duration of 10 days through bipolar electrodes placed bilaterally in lateral hypothalamus and substantia nigra--ventral tegmental area. At the end of 10 days, rats were sacrificed, and rapid Golgi examination of the CA3 hippocampal and layer V pyramidal neurons of the motor cortex was made for a grand total of 1600 neurons from 80 rats divided into 4 groups. The neurons of the self-stimulation experienced (SS) group revealed a significant (ANOVA, F-test) increase in dendritic branching in the perisomatic domains. Such changes were not observed in neurons of sham control (SH), experimenter administered stimulation (EA) and normal control (NC) groups. SS animals also showed a significant increase in the thickness of lacunosum and radiatum laminae of CA3 neurons of the hippocampus. Our results reveal that both limbic and neocortical neurons undergo changes in dendritic branching patterns due to self-stimulation rewarding experience. It is tempting to hypothesize that neuronal plasticity is the result of motivation and learning experienced by rats which underwent self-stimulation.
Responses of aging brain to physical training was evaluated by quantifying the substrates, glucose, lactic acid, and nucleic acids in cerebral cortex (CC) and medulla oblongata (MO) of the brain in rats. Rats of 1 month (young), 6 months (adult), 12 months (middle-aged) and 18 months (old) of age were swim-trained for 30 days. Glucose content of CC and MO increased with training whereas blood glucose decreased in trained young and adult animals with middle-aged and old animals maintaining constant blood glucose. Brain lactate in these two regions decreased with training in all age groups. However, the old animals showed an elevation in blood lactic acid in trained state, while the other age groups showed a decrease. Nucleic acid content, decreased with age, especially the RNA content in MO showing a larger depletion. However, there was no discernible influence of physical exercise on these parameters. Physical training has influenced the aging brain's adaptability, as seen by increase in its glucose content in young animals and also possible utilization of lactate as an additional substrate in old animals as evidenced by an increase in blood lactic acid.
The role of the entorhinal cortex (EC) in stress-induced damage in terms of dendritic branching points and intersections of hippocampal CA3 neurons has been investigated. Following bilateral electrolytic lesions of the EC, the rats were subjected to restraint stress, 6 h per day for 21 days. Chronic restraint stress resulted in the atrophy of hippocampal CA3 neurons and the lesioning of the EC prior to stress significantly (P < 0.001) reduced this dendritic atrophy. These results show that the neuronal vulnerability to chronic stress can be attenuated by entorhinal glutamatergic denervation.
The mechanism by which (-) deprenyl enhances cognitive function in Alzheimer's disease (AD) is not yet understood. (-) Deprenyl (0.2 mg/kg/day) was administered intramuscularly to adult male monkeys (n = 6) for 25 days. Control monkeys (n = 6) received physiological saline by the same route. The activity of acetylcholinesterase (AChE) in different brain regions and the dendritic arborization in CA3 pyramidal neurons of hippocampus were analysed. (-) Deprenyl-treated monkeys showed a significant increase in the AChE activity by 43% (p < 0.001) in the frontal cortex, by 39% (p < 0.025) in the motor cortex, by 66% (p < 0.001) in the hippocampus and by 26% (p < 0.05) in the striatum compared to controls. The branching points and the intersections of both apical and basal dendrites of CA3 hippocampal pyramidal neurons were also significantly increased in (-) deprenyl-treated monkeys. Enhanced AChE activity may increase dendritic arborization in the hippocampus and it may also play a role in improving cognitive functions observed in AD, following (-) deprenyl treatment.
Self-stimulation (SS) rewarding experience induced structural changes in CA3 hippocampal and layer V motor cortical pyramidal neurons in adult male Wistar rats has been demonstrated. In the present study, whether these structural changes are transient or of a permanent nature was evaluated. Self-stimulation experience was provided for 1 h daily over a period of 10 days through bilaterally implanted bipolar electrodes in the lateral hypothalamus and the substantia nigra-ventral tegmental area. Following 10 days of SS experience, the rats were sacrificed after an interval of 30 and 60 days for the quantitative analysis of the dendritic morphology in Golgi stained CA3 hippocampal and layer V motor cortical pyramidal neurons. The results revealed a significant increase in the dendritic branching points and intersections in apical and basal dendrites in both types of neurons in 30 days post-SS group compared to sham control. The total number of apical and basal dendrites were significantly increased in both 30 and 60 days post-SS groups of rats. This study suggests that SS experience induced structural changes are sustainable, even in the absence of rewarding experience.
Intracranial self-stimulation (ICSS) rewarding experience is known to modulate learning and memory and induce morphological and neurochemical changes in hippocampus. Therefore, we studied the effect of ICSS on the hippocampus-dependent operant and the spatial learning tasks in rats with bilateral electrolytic lesioning of fornix. Bilateral lesioning of fornix induced deficits in acquisition and performance of both the tasks, whereas exposure to 10 days of ICSS experience from ventral tegmental area reversed these behavioural deficits. Hence, we propose that the ICSS experience ameliorates the fornix lesion induced behavioural deficits, by inducing neuronal plasticity in the hippocampus which may act as a compensatory mechanism for the deficits produced by the lesioning of fornix.
Dementia, and Alzheimer's disease in particular, is one of the principal causes of disability and decreased quality of life among the elderly and a leading obstacle to successful aging.1,2 In the next 50 years, the prevalence of Alzheimer's disease in the United States is projected nearly to quadruple — which means that 1 in every 45 Americans will be afflicted with the disease.3 This dramatic increase in prevalence will result primarily from the aging of the population. The percentage of Americans older than 75 years of age is predicted to increase from approximately 5.9 percent in 2000 to 11.4 . . .
The heart faces a high risk of free radical injury owing to a slow generation of antioxidant (AO) enzymes by its cells. A general decline in this system may be another reason for the development of age-related diseases. Although the correlation between aging and exercise has been studied extensively, these studies have produced conflicting data on the effects of vitamin E on the aging heart, when it is introduced as an intervening factor. To investigate these effects, we determined the activities of antioxidant enzymes (AOEs) such as superoxide dismutase (SOD) and catalase (CAT), lipid peroxidation (LP), lipofuscin (LF)-like autofluorescent substances and vitamin E content in the left and right ventricles (LV and RV) of the heart in male Wistar albino rats of 4-(young adults), 8-(old adults), 12-(middle-age) and 22-mos(old) of age. Animals were orally supplemented with vitamin E and allowed to swim for 30 min/day, 5 days/week and for a total period of 60 days. Exercise training in all the age groups except the old was effective in upregulating the SOD activity. Old trainees showed an increase in SOD activity when supplemented with vitamin E. In the 22-mo-olds, a remarkable decrease in CAT activity was seen. Exercise by itself upregulated the CAT as well as SOD activity in all age groups except the old wherein vitamin E was effective in increasing the activities of AOEs. Supplementation significantly reduced LP as evidenced by lowered malondialdehyde (MDA) and LF-like autofluorescent substances in the trained as well as sedentary rats. Tissue vitamin E content was low in the swim trainees that were not supplemented. This change, well emphasized in the trainee groups of 22-mo-old suggests the probable utilization of vitamin E in keeping free radicals at bay. Our results suggest that vitamin E can stand out as a significant tool in ameliorating the declining AO defense in the old rats.
An MRI method for quantification of cerebral blood volume (CBV) in time-course studies of angiogenesis is described. Angiogenesis was stimulated by acclimation to hypoxia. The change in relaxation rate, R2, which is relatively sensitive to the microvasculature, was quantified before and after infusion of a superparamagnetic vascular contrast agent (MION). The DeltaR2 was measured in serum and brain parenchyma with a multiecho sequence. In vitro and in vivo calibration curves of MION concentration vs. R2 were approximated by a linear function. CBV was 3.14 +/- 0.32% (mean +/- SE, n=13) and 6.42 +/- 0.54% (n=4) before and after acclimation. A second acclimated group was hemodiluted to control for polycythemia. CBV was not significantly different between hemodiluted and nonhemodiluted groups. In animals where NMR measurements were taken before and after acclimation, there was a 120% increase in CBV. The NMR technique was validated using quantitative morphometrics, which showed an increase of 147% in CBV with acclimation. We found a linear correlation between MRI and the morphometric results for CBV, as well as demonstrating a quantitative equivalence for relative changes in CBV. This article describes a simple, repeatable method of imaging brain microvascular volume using a plasma-based contrast agent that can be applied to longitudinal studies of angiogenesis.
Exercise modulates many aspects of physiology. The purpose of the current experiment was to characterize the impact of regular, moderate physical activity on resting, baseline measures of cellular immunity blood lipids, and muscle enzyme.
Male Fischer 344 rats were housed with either mobile (run, N = 10) or immobile (sedentary, N = 10) running wheels. After 4 wk of running, rats were sacrificed. Blood and muscle (long and medial heads of the triceps) were collected. From blood, white blood cell (WBC) differentials, red blood cell (RBC) count, hemoglobin, hematocrit, and lipid profiles were measured. Muscle citrate synthase (CS) activity was measured by spectrophotometric analysis.
Rats ran an average of 9.89 +/- 0.79 km.wk(-1). There were no differences in the total number of circulating WBC, RBC, or eosinophils. Freewheel running decreased the number of circulating neutrophils (P < 0.001), monocytes (P < 0.01), and basophils (P < 0.01), while increasing the number of lymphocytes (P < 0.001), when compared with sedentary animals. Mean corpuscular content of hemoglobin was elevated in the freewheel group (P < 0.01). Physically active animals had slightly lower triglycerides and LDL, and elevated HDL. These changes resulted in a significant improvement in LDL/HDL ratio (P < 0.05). Muscle CS activity was unchanged between groups.
Both the alterations in the RBC hemoglobin and lipid proteins are positive health changes associated with exercise training. The impact of the alterations in WBC differentials remains unknown but could indicate a reduction in inflammatory load. In conclusion, freewheel running provides sufficient exercise stimulus to produce some, but not all, training associated physiological adaptations.
Physical activity has been shown to be positively associated with cognitive health, but the mechanisms underlying the benefits of physical activity on cognitive health are unclear. The present study simultaneously examined two hypotheses using structural equation modeling (SEM). The depression-reduction hypothesis states that depression suppresses cognitive ability and that physical activity alleviates dysphoric mood and thereby improves cognitive ability. The social-stimulation hypothesis posits that social contact, which is often facilitated by socially laden physical activities, improves cognitive functioning by stimulating the nervous system. Sedentary behavior in the absence of physical activity is expected to exert an inverse relationship on cognitive health through each of these hypotheses. Community-dwelling elders (N = 158) were administered a variety of measures of cognition, depression, social support, and physical activity. SEM techniques provided partial support for the social-stimulation hypothesis and depression-reduction hypothesis. Implications for treating depression and improving cognitive functioning are discussed.