the world health organization ( who ) defines overweight and obesity as body mass index ( bmi )  25 and bmi  30 , respectively . around the world , obesity has become a worrying health and social issue , threatening lives of thousands of people . according to the who , over 1.9 billion adults ( 39% adults ) were overweight among which more than 600 million ( 13% adults ) were obese . childhood obesity is also common that 42 million children were overweight or obese in 2013 . considering its high prevalence , it is pressing to study the pathogenesis , manifestations , and prevention of obesity . obesity is related to a range of health - related problems , such as diabetes , heart disease , hypertension , and cancer . obese children show greater cardiovascular risk factors and persistence of obesity into their adulthood , which may be associated with higher likelihood of premature mortality [ 4 , 5 ] . in addition to health problems , obesity is associated with poorer cognition and motor control , and altered brain plasticity . in this review , we first look into the behavioral manifestations of obese individuals ' cognition and motor control capabilities . , the effects of physical exercise to combat obesity and obesity - related deficits in cognition and motor control will also be described . overweight and obesity are usually related to poorer cognition across lifespan [ 68 ] ; however , the association between bmi and cognitive function is weaker in old age [ 9 , 10 ] , partly due to inaccurate adiposity measurement in the aged people . indirect evidence has shown an association between western high fat diet and impaired cognitive functions . based on bmi data , individuals who are overweight or obese fall in the lowest quartile of global cognition , verbal fluency , delayed recall , immediate logical memory , and intelligence . other than bmi , other adiposity measures are also related to cognitive performance and brain changes . there is also a negative correlation between waist - to - hip ratio and hippocampal volume and a positive correlation between waist - to - hip ratio and white matter hyperintensities . compared to bmi , central adiposity has a stronger association with the risk of developing cognitive impairment and dementia in women . hence , studies using bmi as the only indicator of obesity may not be sensitive enough to capture obesity - induced cognitive dysfunctions . neuroimaging studies demonstrate atrophy in the frontal lobes , anterior cingulate gyrus , hippocampus , and thalamus in older obese individuals . bmi increase is associated with lower metabolic activity in the prefrontal cortex and cingulate gyrus , smaller gray matter volume in many brain regions ( particularly prefrontal cortex ) , and deficient white matter integrity in the uncinated fasciculus which is a structure connecting the frontal and temporal lobes [ 1822 ] . smaller gray matter volume in the left orbitofrontal region is related to poorer executive performance in obese women . childhood obesity is related to the reduced executive function , attention , mental rotation , mathematics , and reading achievement [ 2325 ] . obese adolescents have deficits in a range of cognitive functions , such as attention and executive functions [ 26 , 27 ] . an animal study shows that high fat diet induces similar morphometric and metabolic changes in juvenile and adult mice ; however , only early exposure to high fat diet hurts relational memory flexibility and decreases neurogenesis . people with higher midlife bmi have lower global cognition than their thinner counterparts   and midlife obesity is related to the accelerated cognitive aging , but this association is weaker in older adulthood . both age and bmi contribute independently to decreased brain volume in middle and older adulthood . it is more likely for an older adult to have lower cognitive abilities if he / she was overweight or obese during middle age [ 32 , 33 ] . midlife obesity is related to an increased pace of deterioration in executive functions and an increase in waist - to - hip ratio is associated with substantial reduction in total brain volume . lower bmi and waist circumference and higher fat - free mass are associated with slower cognitive decline . midlife overweight / obesity , particularly with metabolic abnormality , is associated with higher dementia risk in older adulthood [ 33 , 3640 ] . moreover hence , midlife is a critical period in which the overweight / obese status can predict one 's cognitive functions and brain health in later life . besides cognition , obesity also affects motor control capabilities , degrading daily functions and health . children who are obese or overweight are poorer in gross and fine motor control and have delayed motor development [ 4450 ] . obese girls of 6th and 7th grades participate in less physical activity and have lower enjoyment of physical activity . children with high bmi have lower level of run which is a fundamental motor skill based on which complex motor skills are learned . observe that the prevalence of mastery of all fundamental motor skills is lower in overweight / obese children , especially for run , slide , hop , dribble , and kick . in addition to bmi , waist circumference is also related to children 's and adolescents ' ability to perform fundamental motor skills . there is an inverse relationship of bmi with fine motor precision , balance , running speed and agility , and strength in the 1st graders . obese children also have difficulty in postural coordination and a heightened dependency on vision during locomotion which is rather automatic in nonobese children [ 57 , 58 ] . adiposity is related to muscle quality ratio that is associated with motor conduction velocity and finger tapping speed . subcutaneous fatness can account for a significant variance of health - related and motor fitness . excessive fat mass is associated with poorer posture and walking . in middle and older adults , a combination of high bmi ( or waist circumference ) and high blood pressure is related to lower motor speed and manual dexterity . during postural control , obese individuals require greater attention resources to maintain balance during unipedal stance ; this implicates that obese people consume attention resources to compensate for their motor deficits . for example , obesity may affect brain structure , leptin and insulin dysregulation , oxidative stress , cerebrovascular function , blood - brain barrier , and inflammation [ 11 , 6571 ] . some also suggest that obesity - related changes in metabolism interact with age to impair brain functions . in terms of brain structure , obese individuals have lower cortical thickness in the left superior frontal and right medial orbitofrontal cortex . there is also a negative relationship between neuronal injury and gray matter density in hippocampus and cerebellum in overweight and obese individuals . it is suggested that the medial orbitofrontal cortex , hippocampus , and cerebellum are involved in reward - based learning , memory , and motor control and learning [ 7577 ] ; structural alterations in these regions may be associated with deficits in cognitive and motor domains . diet - induced obesity promotes reactive oxygen species in the brain which is associated with both body weight and adiposity [ 79 , 80 ] . in children , occurrence of 15-week obesity during childhood can induce permanent epigenetic changes in rat 's brain . in rats , triglycerides diminish the passage of insulin - like growth factors ( igfs ) into the brain through cerebrospinal fluid , impair hippocampal long - term potentiation , and impede leptin transportation across the blood - brain barrier [ 8385 ] . juvenile exposure to high fat diet impairs long - term spatial memory , but not short - term memory , suggesting a selective impairment of consolidation which is likely contributed by increased proinflammatory cytokine expression in the hippocampus . moreover , consumption of western diet is thought to degrade blood - brain barrier , which consequently damages hippocampus and leads to dementia . relative to those having normal diet , mice consuming high fat diet for 17 days develop insulin resistance in cerebral cortex tissues , degraded synaptic integrity , and poorer spatial memory . it can cross the blood - brain barrier and binds to presynaptic gabaergic neurons to produce its effects [ 89 , 90 ] . as leptin receptors are widespread in the brain ( e.g. , throughout the cortex and the hippocampus ) , leptin can modulate memory processes . obese mice with impaired leptin signaling have deficits of hippocampal - dependent memory   and increased basal hippocampal inflammation [ 94 , 95 ] . leptin is related to neurogenesis , axonal growth , and synaptogenesis in addition to hypothalamic functions [ 9698 ] . for hippocampal neurons , leptin plays a role in long - term potentiation and depression and thus is important for synaptic plasticity [ 92 , 99 , 100 ] . compared to those with low leptin level , the elderly with high leptin level show less cognitive decline during aging . high leptin level in individuals with small waist circumference is related to less cognitive decline over 10 years . the presence of leptin may decrease the production of amyloid and speed up the removal of -amyloid . obese individuals usually develop leptin resistance   which results in an increase in food intake and alteration of energy expenditure . the circulating levels of insulin and signaling pathway are altered in obesity ; this interacts with inflammatory processes to modulate cognition and behaviors . insulin receptors are widespread in hippocampal and cortical brain structures , insulin signaling can contribute to the formation of declarative memory . insulin concentrations vary with adiposity and there is a negative relationship between the amount of visceral fat and insulin sensitivity . insulin resistance can result from high fat consumption or obesity [ 110 , 111 ] . dysfunctional insulin signaling can induce inflammation and promote -amyloid and tau pathology , contributing to neurodegeneration [ 112 , 113 ] . insulin resistance can mediate cognitive impairment and neurodegeneration as insulin and igfs can regulate neuronal survival , metabolism , and brain plasticity [ 114 , 115 ] . during insulin resistance , there is a failure of cells to metabolize glucose , which consequently triggers an increase of insulin level . insulin signaling is related to tau phosphorylation , an early pathology of alzheimer 's disease [ 116 , 117 ] ; this is complementary to the fact that there are a large number of insulin - sensitive glucose transporters in the medial temporal lobe . thus , insulin dysregulation in the obese people likely confers a greater risk of dementia to them . the adipose tissue produces many substances for metabolism ( adipokines , such as bdnf ) and inflammation ( cytokines , such as leptin ) . many cytokines , such as interleukin-1 , produced by the adipose tissue can cross the blood - brain barrier and affect cognitive functions through neuroinflammation [ 95 , 119 ] . similar to leptin , it exerts its effects in the brain to bring about weight reduction . reduced hippocampal adiponectin levels are observed in aging animals , independent of high fat diet intake . neurotrophins , such as igf-1 and bdnf , can mediate obesity 's effects on cognition and behaviors . igf-1 is mainly produced in liver and binds to the igf-1 or insulin receptors to exert its effects to stimulate cell growth and proliferation and promote -amyloid clearance in the brain . obese individuals usually show igf-1 resistance , degrading their capability to prevent -amyloid deposition and neurodegeneration [ 114 , 123 ] . besides , bdnf can bind to many receptors , such as trkb and lngf receptors , to support neuronal survival and stimulate neurogenesis and synaptogenesis [ 124126 ] . bdnf promotes neuronal differentiation and survival , neurogenesis , and brain plasticity and is thus particularly crucial for learning and memory . high fat diet reduces bdnf level in the hippocampus , and the impaired hippocampal synaptic plasticity and cognition are possibly through bdnf 's effects on dendritic spines . diet - induced obesity reduces hippocampal expression of bdnf and presynaptic synaptophysin , which are related to an impairment of spatial learning in mice . although mounting evidence shows that obesity is associated with structural and functional brain changes , the causal link between them requires further investigations . the composition of gut microbiota appears to be causally related to obesity [ 132134 ] , playing a significant role in body weigh regulation since birth [ 135 , 136 ] . gut microbiota plays a key role in childhood obesity and brain development [ 137 , 138 ] . a comparison of germ - free mice and conventionally reared mice has demonstrated that germ - free mice are leaner and more resistant to diet - induced obesity . obese and nonobese individuals have different diversity and composition of gut microbiota [ 140 , 141 ] . as gut microbiota controls energy extraction and storage in the body , significant changes in gut microbiota can result in obesity and insulin resistance [ 139 , 140 , 142 ] . it has been suggested that diet can influence gut microbiota which in turn impacts the brain and behaviors through neural , hormonal , immune , and metabolic pathways [ 143 , 144 ] . transplantation of gut microbiota of diet - induced obese mice to lean mice is sufficient to bring about neurobehavioral changes through increasing neuroinflammation and disrupting cerebrovascular homeostasis [ 145 , 146 ] . mice consuming high energy diet containing higher percentage of clostridiales and lower expression of bacteroidales have poorer cognitive flexibility . in humans , the firmicutes gut microbiota can modulate a range of neurotrophins , such as bdnf and synaptophysin , to affect neural plasticity [ 149 , 150 ] . thus , diet changes gut microbiota which influences neurophysiology and neurotrophins , eventually impacting cognition and behaviors . previous results have shown that obesity - related brain plasticity alteration is a multifaceted issue , which can inflict permanent harm to individuals in their early ages . thus exercise can improve physical and cognitive performance , and quality of life in the elderly [ 151155 ] . in humans , those who are highly fit or aerobically trained have greater prefrontal and parietal activations for spatial selection and inhibitory functioning . there is a positive relationship between aerobic fitness and spatial memory which is mediated by hippocampus volume . aerobic training can increase hippocampal volume of the elderly ( with or without mild cognitive impairment ) and increases plasma bdnf level in both patients of alzheimer 's disease and healthy controls [ 158163 ] . regular physical activity is related to better cognition , less cognitive decline , and a lower risk of developing dementia [ 164 , 165 ] . as young as children , aerobic fitness can predict cognitive performance over time . besides cognition , higher level of physical activity is related to a reduced white matter hyperintensity burden on motor function in the aged people . lifelong exercise can preserve white matter microstructure related to motor control and coordination in the elderly . in addition , regular physical activity has long been suggested to be an effective way to improve obesity and related problems [ 170 , 171 ] . exercising 5 days per week for 15 weeks can improve executive functions in overweight children . high - intensity physical activity ( both aerobic and endurance training ) for 4 months improves cognition and oxygen extraction in obese individuals . the effectiveness of exercise may be moderated by exercise intensity and duration , and exerciser 's developmental stage [ 174 , 175 ] . exercise intensity can be related both to behavioral outcomes and to changes in brain structure and bdnf level . greater amount of physical activity in early life is associated with larger prefrontal and hippocampal volumes . individuals receiving low - intensity exercise , but not high - intensity , show increased bdnf expression . bdnf level depends on exercise intensity ; some observe that moderate - intensity exercise is the most effective to promote bdnf in the elderly . fail to observe any augmentation of task switching performance after a single bout of moderately intense exercise . in midlife mice , only 4-month ( but not 2-month ) running training can trigger activation of the antiamyloidogenic , prosurvival , synaptogenic , and neuroprotective pathways . wheel running for 14 days can increase cell proliferation in the dentate gyrus whereas wheel running for 56 days can additionally facilitate long - term potentiation in this region . four - week exercise can improve recognition memory in adult rats , but no such enhancement can be recorded 2 weeks after cessation of training . however , in adolescent rats , the enhancement of recognition memory is preserved . , physical activity can enhance neurogenesis , neuroadaptation , and neuroprotection though the actions of neurotrophic factors [ 184190 ] . hippocampal function is restored by physical activity through enhancing the expression of neurotrophic factors to promote neurogenesis , angiogenesis , and synaptic plasticity [ 191193 ] . for example , bdnf level increases with physical activity , particularly regular exercise [ 194 , 195 ] . it is found that bdnf can stimulate dna repair to protect cortical neurons against oxidative stress . short bout of mild exercise for 5 weeks improves both oxygen consumption and long - term spatial learning and memory in aged rats which is associated with hippocampal bdnf level . following physical activity , the elevated bdnf level in the dentate gyrus is sufficient to induce spatial memory improvement . a week of voluntary exercise is sufficient to increase the activity of tissue type plasminogen activator to facilitate the cleavage of probdnf into mbndf . a 7-day exercise intervention can increase gray matter volumes in the motor , somatosensory , association , and visual cortices in rats . exercising for 6 months reduces default mode network activity in the precuneus   while one - year walking increases functional connectivity within the default mode network and frontal executive network . regular physical activity can reduce proinflammatory and increase anti - inflammatory signaling and reduce oxidative stress in aged animals [ 206 , 207 ] . exercise also reduces peripheral risk factors , such as diabetes and cardiovascular diseases which are associated with neurodegeneration . furthermore , vasculature is altered after exercise . in middle - aged rats , total length and surface area of cortical capillaries aerobic exercise at midlife can improve vascular dysfunctions , astrocyte hypertrophy , and myelin dysregulation associated with sedentary lifestyle [ 210 , 211 ] . exercise is associated with a range of improvements in the brain through a range of mechanisms in individuals of different weight statuses ( figure 1 ) . the effectiveness of exercise depends on the training parameters , such as intensity , duration , and developmental stage of exerciser . previous research results have consistently suggested that moderately intense exercise for a long enough period of time is especially beneficial for young exercisers . more and more people are becoming obese , producing aversive effects on their cognition , motor behaviors , and quality of life . previous research has suggested that altered brain structure and activation mediate obesity 's influences on cognition [ 1721 ] , whereas obesity influences the musculoskeletal system to degrade motor performance . as motor performance partly depends on cognitive ability , obesity may indirectly contribute to motor deficits through cognitive decline ( figure 1 ) . substantial research has shown that obesity affects our cognition and motor behaviors through different mechanisms , possibly through altering brain structure , leptin / insulin regulation , oxidative stress , cerebrovascular function , blood - brain barrier , and inflammation [ 11 , 6571 ] . it is suggested that moderately intense exercise for a long enough period of time seems favorable ; however , the training parameter for optimal outcomes remains to be determined . most of the previous research focuses on aerobic exercise ; the efficacy of anaerobic exercise to improve obesity and related dysfunctions is not well understood . more efforts should be devoted to investigate the efficacy of anaerobic exercise , in comparison with aerobic exercise . moreover , starting exercising in young age is particularly important to protect from neurodegeneration in old age . as childhood obesity is becoming more prevalent [ 2325 ] , introducing physical activity intervention in childhood may help children improve obesity and prevent age - related functional decline in old age . in addition to exercise , leptin replacement therapy , inhaled insulin therapy , and caloric restriction have also been proposed to improve obesity . leptin is responsible for energy balance and body weight and can affect neurogenesis and brain functions . it is observed that 18-month leptin replacement therapy increases gray matter concentration and activations in brain regions implicated in hunger and satiation neural circuits [ 213 , 214 ] . during weight loss , it is found that intranasal insulin exerts anorexic effects , promoting satiety and regulating food intake [ 219 , 220 ] . inhaled insulin reaches the brain through olfactory nerves and specific receptors in blood - brain barrier to exert its effects . caloric restriction also improves obesity and reverses deficits in leptin receptor protein and signaling associated with diet - induced obesity . after 3 months of caloric restriction , serum bdnf increases in overweight and obese individuals . diet - induced weight loss is related to a decrease in plasma free fatty acid and improvement in episodic memory . hitherto , the efficacy of leptin replacement therapy , inhaled insulin therapy , and caloric restriction on cognition and motor behaviors is poorly understood , which warrants further verification . it affects cognition mainly through altering the brain structures and functions [ 1721 ] , and motor performance through degrading musculoskeletal system . obesity can affect brain structure , leptin / insulin dysregulation , oxidative stress , cerebrovascular function , blood - brain barrier , and inflammation [ 11 , 6571 ] , which are involved in the deterioration of cognitive and motor functions . a host of previous research has suggested that exercise can improve both obesity - related cognitive and motor declines . as more and more people develop obesity in young age , introducing exercise intervention
due to a sedentary lifestyle , more and more people are becoming obese nowadays . 
 in addition to health - related problems , obesity can also impair cognition and motor performance . 
 previous results have shown that obesity mainly affects cognition and motor behaviors through altering brain functions and musculoskeletal system , respectively . 
 many factors , such as insulin / leptin dysregulation and inflammation , mediate the effect of obesity and cognition and motor behaviors . 
 substantial evidence has suggested exercise to be an effective way to improve obesity and related cognitive and motor dysfunctions . 
 this paper aims to discuss the association of obesity with cognition and motor behaviors and its underlying mechanisms . following this , 
 mechanisms of exercise to improve obesity - related dysfunctions are described . 
 finally , implications and future research direction are raised .