تغییر ساختاری #قشرمخ در مواجهه با #دیستایمی (اختلال #افسردگی #خفیف/#ملال)
Evidence for #neuroplastic compensation in the #cerebral #cortex of persons with #depressive illness
پژوهش های جدید نشان داده اند که #ساختار قشر مخ در افراد دارای افسردگی خفیف (دیستایمی) متفاوت از افراد غیر افسرده است و این تفاوت با #دارودرمانی مناسب برطرف می شود.
در افراد دارای دیستایمی ضخامت قشر مخ نسبت به افراد عادی بیشتر می شود (#هایپرتروفی #کرتکس) که در این پژوهش با #Duloxetine بعنوان دارودرمانی، کاهش ضخامت به اندازه عادی در این افراد در دوره 10 هفته ای مشاهده شد.
Abstract
We yoked #anatomical #brain magnetic resonance imaging (#MRI) to a #randomized, #double-blind, #placebo-#controlled trial (#RCT) of #antidepressant medication for 10-week’s duration in patients with #dysthymia. The RCT study design mitigated ascertainment bias by randomizing patients to receive either #duloxetine or #placebo, and it supported true causal inferences about treatment effects on the brain by controlling treatment assignment experimentally. We acquired 121 #anatomical #scans: at #baseline and end point in 41 patients and once in 39 healthy controls. At baseline, patients had diffusely thicker cortices than did healthy participants, and patients who had thicker cortices had proportionately less severe symptoms. During the trial, symptoms improved significantly more in medication—compared with placebo-treated patients; concurrently, thicknesses in medication-treated patients declined toward values in healthy controls, but they increased slightly, away from control values, in placebo-treated patients. Changes in symptom severity during the trial mediated the association of treatment assignment with the change in thickness, suggesting that the beneficial effects of medication on symptom severity were at least partially responsible for normalizing cortical thickness. Together our findings suggest that baseline cortical #hypertrophy in medication-free patients likely represented a compensatory, #neuroplastic #response that attenuated symptom severity. #Medication then reduced symptoms and lessened the need for compensation, thereby normalizing thickness. This is to the best of our knowledge the first study to report within an RCT a differential change in cortical morphology during medication treatment for depressive illness and the first to provide within an RCT in #vivo evidence for the presence of #neuroanatomical #plasticity in humans.
لینک منبع 👇🏻(read more)👇🏻
http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201734a.html
✅(در صورت جذابیت و علاقمندی به موضوع، مطلب را برای دیگران نیز بازنشر فرمایید).
📢کانال #دکترامیرمحمدشهسوارانی
🍃🌹🌸💐🌸🌹🍃
@DrAmirMohammadShahsavarani
Evidence for #neuroplastic compensation in the #cerebral #cortex of persons with #depressive illness
پژوهش های جدید نشان داده اند که #ساختار قشر مخ در افراد دارای افسردگی خفیف (دیستایمی) متفاوت از افراد غیر افسرده است و این تفاوت با #دارودرمانی مناسب برطرف می شود.
در افراد دارای دیستایمی ضخامت قشر مخ نسبت به افراد عادی بیشتر می شود (#هایپرتروفی #کرتکس) که در این پژوهش با #Duloxetine بعنوان دارودرمانی، کاهش ضخامت به اندازه عادی در این افراد در دوره 10 هفته ای مشاهده شد.
Abstract
We yoked #anatomical #brain magnetic resonance imaging (#MRI) to a #randomized, #double-blind, #placebo-#controlled trial (#RCT) of #antidepressant medication for 10-week’s duration in patients with #dysthymia. The RCT study design mitigated ascertainment bias by randomizing patients to receive either #duloxetine or #placebo, and it supported true causal inferences about treatment effects on the brain by controlling treatment assignment experimentally. We acquired 121 #anatomical #scans: at #baseline and end point in 41 patients and once in 39 healthy controls. At baseline, patients had diffusely thicker cortices than did healthy participants, and patients who had thicker cortices had proportionately less severe symptoms. During the trial, symptoms improved significantly more in medication—compared with placebo-treated patients; concurrently, thicknesses in medication-treated patients declined toward values in healthy controls, but they increased slightly, away from control values, in placebo-treated patients. Changes in symptom severity during the trial mediated the association of treatment assignment with the change in thickness, suggesting that the beneficial effects of medication on symptom severity were at least partially responsible for normalizing cortical thickness. Together our findings suggest that baseline cortical #hypertrophy in medication-free patients likely represented a compensatory, #neuroplastic #response that attenuated symptom severity. #Medication then reduced symptoms and lessened the need for compensation, thereby normalizing thickness. This is to the best of our knowledge the first study to report within an RCT a differential change in cortical morphology during medication treatment for depressive illness and the first to provide within an RCT in #vivo evidence for the presence of #neuroanatomical #plasticity in humans.
لینک منبع 👇🏻(read more)👇🏻
http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201734a.html
✅(در صورت جذابیت و علاقمندی به موضوع، مطلب را برای دیگران نیز بازنشر فرمایید).
📢کانال #دکترامیرمحمدشهسوارانی
🍃🌹🌸💐🌸🌹🍃
@DrAmirMohammadShahsavarani
#شناسایی #سازوکارهای بالقوه ایجاد #الکلیزم
#Dopamine #Neurons #Change the #Type of #Excitability in #Response to #Stimuli
#پژوهشگران مدرسه عالی اقتصاد روسیه با همکاری موسسه ملی سلامت و وزارت آموزش روسیه 🇷🇺، دانشکده نرمال سوپریر فرانسه 🇫🇷، و دانشگاه ایندیانای ایالات متحده 🇺🇸، در پژوهش بر ریشه های #عصبی، #ژنتیک و #متابولیک #الکلیزم در افراد دریافتند که مکانیزم های #تغییریافته عمل در پاسخ #نورون های #دوپامینرژیک در پویایی های #کرتکس #پیش_پیشانی منجر به تغییر سطح #دوپامین مغز شده و فرد را به سمت الکلیزم سوق دهند.
Abstract
#The #dynamics of #neuronal #excitability #determine the #neuron’s response to stimuli, its #synchronization and #resonance properties and, ultimately, the computations it performs in the #brain. We investigated the dynamical #mechanisms underlying the excitability type of dopamine (#DA) neurons, using a #conductance-based #biophysical model, and its #regulation by intrinsic and #synaptic currents. #Calibrating the model to reproduce low frequency #tonic firing results in #N-methyl-D-aspartate (#NMDA) #excitation balanced by γ-Aminobutyric acid (#GABA)-mediated #inhibition and leads to type I excitable behavior characterized by a continuous decrease in firing frequency in response to #hyperpolarizing currents. Furthermore, we analyzed how excitability type of the DA neuron model is influenced by changes in the intrinsic current composition. A #subthreshold #sodium current is necessary for a continuous frequency decrease during application of a negative current, and the low-frequency “balanced” state during simultaneous activation of NMDA and GABA #receptors. Blocking this current switches the neuron to type II characterized by the abrupt onset of repetitive firing. Enhancing the #anomalous rectifier #Ih current also switches the excitability to type II. Key characteristics of synaptic conductances that may be observed in vivo also change the type of excitability: a #depolarized γ-Aminobutyric acid receptor (#GABAR) reversal potential or co-activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (#AMPARs) leads to an abrupt frequency drop to zero, which is typical for type II excitability. Coactivation of N-methyl-D-aspartate receptors (#NMDARs) together with AMPARs and GABARs shifts the type I/II boundary toward more hyperpolarized GABAR reversal potentials. To better understand how altering each of the aforementioned currents leads to changes in excitability profile of DA neuron, we provide a thorough dynamical analysis. Collectively, these results imply that type I excitability in dopamine neurons might be important for low firing rates and fine-tuning basal dopamine levels, while switching excitability to type II during NMDAR and AMPAR activation may facilitate a transient increase in dopamine concentration, as type II neurons are more amenable to synchronization by mutual excitation.
لینک منبع 👇🏻(further reading)👇🏻
journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1005233
✅(در صورت جذابیت و علاقمندی به موضوع، مطلب را برای دیگران نیز بازنشر فرمایید).
📢کانال #دکترامیرمحمدشهسوارانی
🍃🌹🌸💐🌸🌹🍃
@DrAmirMohammadShahsavarani
#Dopamine #Neurons #Change the #Type of #Excitability in #Response to #Stimuli
#پژوهشگران مدرسه عالی اقتصاد روسیه با همکاری موسسه ملی سلامت و وزارت آموزش روسیه 🇷🇺، دانشکده نرمال سوپریر فرانسه 🇫🇷، و دانشگاه ایندیانای ایالات متحده 🇺🇸، در پژوهش بر ریشه های #عصبی، #ژنتیک و #متابولیک #الکلیزم در افراد دریافتند که مکانیزم های #تغییریافته عمل در پاسخ #نورون های #دوپامینرژیک در پویایی های #کرتکس #پیش_پیشانی منجر به تغییر سطح #دوپامین مغز شده و فرد را به سمت الکلیزم سوق دهند.
Abstract
#The #dynamics of #neuronal #excitability #determine the #neuron’s response to stimuli, its #synchronization and #resonance properties and, ultimately, the computations it performs in the #brain. We investigated the dynamical #mechanisms underlying the excitability type of dopamine (#DA) neurons, using a #conductance-based #biophysical model, and its #regulation by intrinsic and #synaptic currents. #Calibrating the model to reproduce low frequency #tonic firing results in #N-methyl-D-aspartate (#NMDA) #excitation balanced by γ-Aminobutyric acid (#GABA)-mediated #inhibition and leads to type I excitable behavior characterized by a continuous decrease in firing frequency in response to #hyperpolarizing currents. Furthermore, we analyzed how excitability type of the DA neuron model is influenced by changes in the intrinsic current composition. A #subthreshold #sodium current is necessary for a continuous frequency decrease during application of a negative current, and the low-frequency “balanced” state during simultaneous activation of NMDA and GABA #receptors. Blocking this current switches the neuron to type II characterized by the abrupt onset of repetitive firing. Enhancing the #anomalous rectifier #Ih current also switches the excitability to type II. Key characteristics of synaptic conductances that may be observed in vivo also change the type of excitability: a #depolarized γ-Aminobutyric acid receptor (#GABAR) reversal potential or co-activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (#AMPARs) leads to an abrupt frequency drop to zero, which is typical for type II excitability. Coactivation of N-methyl-D-aspartate receptors (#NMDARs) together with AMPARs and GABARs shifts the type I/II boundary toward more hyperpolarized GABAR reversal potentials. To better understand how altering each of the aforementioned currents leads to changes in excitability profile of DA neuron, we provide a thorough dynamical analysis. Collectively, these results imply that type I excitability in dopamine neurons might be important for low firing rates and fine-tuning basal dopamine levels, while switching excitability to type II during NMDAR and AMPAR activation may facilitate a transient increase in dopamine concentration, as type II neurons are more amenable to synchronization by mutual excitation.
لینک منبع 👇🏻(further reading)👇🏻
journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1005233
✅(در صورت جذابیت و علاقمندی به موضوع، مطلب را برای دیگران نیز بازنشر فرمایید).
📢کانال #دکترامیرمحمدشهسوارانی
🍃🌹🌸💐🌸🌹🍃
@DrAmirMohammadShahsavarani
journals.plos.org
Dopamine Neurons Change the Type of Excitability in Response to Stimuli
Author Summary Dopamine neurons play a central role in guiding motivated behaviors. However, complete understanding of computations these neurons perform to encode rewarding and salient stimuli is still forthcoming. Network connectivity influences neural…
♻️روشی نوین و کم آسیب برای درمان #صرع های قوی و پایدار
#Differential #temperature #sensitivity of #synaptic and #firing processes in a #neural #mass #model of #epileptic #discharges explains #heterogeneous response of #experimental #epilepsy to #focal #brain #cooling
پژوهشگران نوروساینس انستیتو علوم و تکنولوژی نارا (NAIST) 🇯🇵 در پژوهشی که به تازگی منتشر شده است، به مدل #شبیه سازی شده #کامپیوتری دست یافتند که نشان می دهد چطور می توان بخش های خاصی از #مغز را #خنک کرد؛ این امر رهیافت مهمی در درمان #صرع محسوب می شود.
🔬برای این منظور، بر پایه یافته های حاصل از مدل #موش، ابتدا به شبیه سازی خنک سازی #کانونی برای کاهش فعالیت #نورونی مغز موش پرداخته شد تا مشخص شود چه واکنش هایی را برای کاهش حملات صرع در پی دارد. سپس، سازوکاری به این مدل اضافه شد که خنک سازی منجر به #تخلیه الکتریکی بشود اما شدت آن کمتر باشد.
📚این مدل ترکیبی جدید، رهیافتی نوین برای خنک کردن کانونی مغز است که نسبت به #جراحی آسیبهای جانبی و عوارض بسیار کمتری دارد و نتایج حاصله از آن در کاهش حملات صرع در افراد بسیار بیشتری قابل کاربرد است. در عین حال روش #خنکسازی #موضعی، آسیبی به #بافت های مغزی و عملکردهای نورونی مغز نمی زند.
🔆بطور میانگین، 50 میلیون نفر در جهان مبتلا به انواع #حملات #صرع هستند.
Abstract
#Experiments with #drug-induced #epilepsy in #rat #brains and #epileptic #human brain region reveal that #focal #cooling can suppress epileptic #discharges without affecting the #brain’s normal #neurological #function. Findings suggest a viable treatment for intractable epilepsy cases via an implantable cooling device. However, precise mechanisms by which cooling suppresses epileptic discharges are still not clearly understood. Cooling experiments #in #vitro presented evidence of reduction in #neurotransmitter release from #presynaptic #terminals and loss of #dendritic #spines at #post-synaptic terminals offering a possible synaptic mechanism. We show that termination of epileptic discharges is possible by introducing a #homogeneous #temperature factor in a neural mass model which attenuates the post-synaptic impulse responses of the neuronal populations. This result however may be expected since such attenuation leads to reduced post-synaptic potential and when the effect on #inhibitory #interneurons is less than on #excitatory interneurons, #frequency of #firing of #pyramidal #cells is consequently reduced. While this is observed in cooling experiments in vitro, experiments in vivo exhibit persistent discharges during cooling but suppressed in magnitude. This leads us to conjecture that reduction in the frequency of discharges may be compensated through #intrinsic excitability mechanisms. Such compensatory mechanism is modelled using a #reciprocal #temperature #factor in the #firing #response function in the neural mass model. We demonstrate that the complete model can reproduce attenuation of both magnitude and frequency of epileptic discharges during cooling. The compensatory mechanism suggests that cooling lowers the #average and the #variance of the #distribution of #threshold potential of firing across the population. #Bifurcation study with respect to the temperature parameters of the model reveals how heterogeneous response of epileptic discharges to cooling (#termination or #suppression only) is exhibited. Possibility of differential temperature effects on post-synaptic potential generation of different populations is also explored.
لینک منبع 👇🏻(further reading)👇🏻
http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1005736
✅(در صورت جذابیت و علاقمندی به موضوع، مطلب را برای دیگران نیز بازنشر فرمایید).
📢کانال #دکترامیرمحمدشهسوارانی
🍃🌹🌸💐🌸🌹🍃
@DrAmirMohammadShahsavarani
#Differential #temperature #sensitivity of #synaptic and #firing processes in a #neural #mass #model of #epileptic #discharges explains #heterogeneous response of #experimental #epilepsy to #focal #brain #cooling
پژوهشگران نوروساینس انستیتو علوم و تکنولوژی نارا (NAIST) 🇯🇵 در پژوهشی که به تازگی منتشر شده است، به مدل #شبیه سازی شده #کامپیوتری دست یافتند که نشان می دهد چطور می توان بخش های خاصی از #مغز را #خنک کرد؛ این امر رهیافت مهمی در درمان #صرع محسوب می شود.
🔬برای این منظور، بر پایه یافته های حاصل از مدل #موش، ابتدا به شبیه سازی خنک سازی #کانونی برای کاهش فعالیت #نورونی مغز موش پرداخته شد تا مشخص شود چه واکنش هایی را برای کاهش حملات صرع در پی دارد. سپس، سازوکاری به این مدل اضافه شد که خنک سازی منجر به #تخلیه الکتریکی بشود اما شدت آن کمتر باشد.
📚این مدل ترکیبی جدید، رهیافتی نوین برای خنک کردن کانونی مغز است که نسبت به #جراحی آسیبهای جانبی و عوارض بسیار کمتری دارد و نتایج حاصله از آن در کاهش حملات صرع در افراد بسیار بیشتری قابل کاربرد است. در عین حال روش #خنکسازی #موضعی، آسیبی به #بافت های مغزی و عملکردهای نورونی مغز نمی زند.
🔆بطور میانگین، 50 میلیون نفر در جهان مبتلا به انواع #حملات #صرع هستند.
Abstract
#Experiments with #drug-induced #epilepsy in #rat #brains and #epileptic #human brain region reveal that #focal #cooling can suppress epileptic #discharges without affecting the #brain’s normal #neurological #function. Findings suggest a viable treatment for intractable epilepsy cases via an implantable cooling device. However, precise mechanisms by which cooling suppresses epileptic discharges are still not clearly understood. Cooling experiments #in #vitro presented evidence of reduction in #neurotransmitter release from #presynaptic #terminals and loss of #dendritic #spines at #post-synaptic terminals offering a possible synaptic mechanism. We show that termination of epileptic discharges is possible by introducing a #homogeneous #temperature factor in a neural mass model which attenuates the post-synaptic impulse responses of the neuronal populations. This result however may be expected since such attenuation leads to reduced post-synaptic potential and when the effect on #inhibitory #interneurons is less than on #excitatory interneurons, #frequency of #firing of #pyramidal #cells is consequently reduced. While this is observed in cooling experiments in vitro, experiments in vivo exhibit persistent discharges during cooling but suppressed in magnitude. This leads us to conjecture that reduction in the frequency of discharges may be compensated through #intrinsic excitability mechanisms. Such compensatory mechanism is modelled using a #reciprocal #temperature #factor in the #firing #response function in the neural mass model. We demonstrate that the complete model can reproduce attenuation of both magnitude and frequency of epileptic discharges during cooling. The compensatory mechanism suggests that cooling lowers the #average and the #variance of the #distribution of #threshold potential of firing across the population. #Bifurcation study with respect to the temperature parameters of the model reveals how heterogeneous response of epileptic discharges to cooling (#termination or #suppression only) is exhibited. Possibility of differential temperature effects on post-synaptic potential generation of different populations is also explored.
لینک منبع 👇🏻(further reading)👇🏻
http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1005736
✅(در صورت جذابیت و علاقمندی به موضوع، مطلب را برای دیگران نیز بازنشر فرمایید).
📢کانال #دکترامیرمحمدشهسوارانی
🍃🌹🌸💐🌸🌹🍃
@DrAmirMohammadShahsavarani
journals.plos.org
Differential temperature sensitivity of synaptic and firing processes in a neural mass model of epileptic discharges explains heterogeneous…
Author summary Focal cooling of the epileptic brain region has been shown to consistently suppress epileptic activity and it is hoped that this treatment can be developed in the future into an implantable cooling device. However, it is still not clearly understood…
♻️کاربرد #نوروفیدبک #هموگلوبینی برای درمان #چاقی
A #pilot study of a novel #therapeutic approach to #obesity: #CNS modification by #N.I.R. #H.E.G. #neurofeedback
پژوهشگران نوروساینس و تغذیه در گزارشی که به تازگی منتشر شده است به بررسی پایلوت روش جدیدی از نوروفیدبک برای درمان چاقی پرداختند.
🔬در این پژوهش آزمایشی مقدماتی، 6 مرد داوطلب که بجز اضافه وزن و چاقی مشکل دیگری نداشتند به مدت 5 هفته در 10 جلسه تحت درمان نوروفیدبک #NIR #HEG قرار گرفتند و پیش و پس از مداخله، #fMRI، و شاخص های #فیزیولوژیک، #ریخت شناختی و #روانی ایشان ارزیابی شدند.
📚نتایج نشان دادند، این روش نوروفیدبک به #خودکنترلی، #بازداری از خوردن غذا، #کاهش #وزن و افزایش فعالیت مدارهای پاسخ به بازداری #قشر #فوقانی #حدقه ای #پیشانی کمک شایانی می کند.
🔆بر اساس نتایج این پژوهش، نوروفیدبک مبتنی بر سطح هموگلوبین مغزی بهتر از نوروفیدبک مبتنی بر امواج مغزی می تواند در درمان چاقی به افراد کمک کند.
Summary
Background & aims: Despite the thorough #mapping of #brain pathways involved in eating #behavior, no #treatment aimed at modulating #eating #dysregulation from its #neurocognitive root has been established yet. We aimed to evaluate the effect of #N.I.R. #H.E.G. (#Near #Infra-Red #Hemoencephalography) #neurofeedback training on #appetite control, #weight and #food-related brain activity.
Methods: Six healthy male participants with #overweight or mild #obesity went through 10 N.I.R. H.E.G. neurofeedback sessions designed to practice voluntary activation of the #prefrontal #cortex. #Weight, eating behavior, appetite control and brain activity related to food and #self-inhibition based on #fMRI were evaluated before and after neurofeedback training.
Results: Our study group demonstrated a positive trend of increased self-control and inhibition related to food behavior, reduced weight and increased activation during an fMRI #response-inhibition task (#Go-No-Go – GNG) in the predefined #region of #interest (#ROI): #superior #orbitofrontal #cortex (#sOFC).
Conclusions: N.I.R. H.E.G. holds a promising potential as a feasible neurofeedback platform for modulation of #cortical #brain #circuits involved in self-control and eating behavior and should be further evaluated and developed as a brain modifying device for the treatment and prevention of obesity.
لینک منبع پیشنهادی برای مطالعه بیشتر 👇🏻(further reading)👇🏻
https://doi.org/10.1016/j.clnu.2018.01.023
✅(در صورت جذابیت و علاقمندی به موضوع، مطلب را برای دیگران نیز بازنشر فرمایید).
📢کانال #دکترامیرمحمدشهسوارانی
🍃🌹🌸💐🌸🌹🍃
@DrAmirMohammadShahsavarani
A #pilot study of a novel #therapeutic approach to #obesity: #CNS modification by #N.I.R. #H.E.G. #neurofeedback
پژوهشگران نوروساینس و تغذیه در گزارشی که به تازگی منتشر شده است به بررسی پایلوت روش جدیدی از نوروفیدبک برای درمان چاقی پرداختند.
🔬در این پژوهش آزمایشی مقدماتی، 6 مرد داوطلب که بجز اضافه وزن و چاقی مشکل دیگری نداشتند به مدت 5 هفته در 10 جلسه تحت درمان نوروفیدبک #NIR #HEG قرار گرفتند و پیش و پس از مداخله، #fMRI، و شاخص های #فیزیولوژیک، #ریخت شناختی و #روانی ایشان ارزیابی شدند.
📚نتایج نشان دادند، این روش نوروفیدبک به #خودکنترلی، #بازداری از خوردن غذا، #کاهش #وزن و افزایش فعالیت مدارهای پاسخ به بازداری #قشر #فوقانی #حدقه ای #پیشانی کمک شایانی می کند.
🔆بر اساس نتایج این پژوهش، نوروفیدبک مبتنی بر سطح هموگلوبین مغزی بهتر از نوروفیدبک مبتنی بر امواج مغزی می تواند در درمان چاقی به افراد کمک کند.
Summary
Background & aims: Despite the thorough #mapping of #brain pathways involved in eating #behavior, no #treatment aimed at modulating #eating #dysregulation from its #neurocognitive root has been established yet. We aimed to evaluate the effect of #N.I.R. #H.E.G. (#Near #Infra-Red #Hemoencephalography) #neurofeedback training on #appetite control, #weight and #food-related brain activity.
Methods: Six healthy male participants with #overweight or mild #obesity went through 10 N.I.R. H.E.G. neurofeedback sessions designed to practice voluntary activation of the #prefrontal #cortex. #Weight, eating behavior, appetite control and brain activity related to food and #self-inhibition based on #fMRI were evaluated before and after neurofeedback training.
Results: Our study group demonstrated a positive trend of increased self-control and inhibition related to food behavior, reduced weight and increased activation during an fMRI #response-inhibition task (#Go-No-Go – GNG) in the predefined #region of #interest (#ROI): #superior #orbitofrontal #cortex (#sOFC).
Conclusions: N.I.R. H.E.G. holds a promising potential as a feasible neurofeedback platform for modulation of #cortical #brain #circuits involved in self-control and eating behavior and should be further evaluated and developed as a brain modifying device for the treatment and prevention of obesity.
لینک منبع پیشنهادی برای مطالعه بیشتر 👇🏻(further reading)👇🏻
https://doi.org/10.1016/j.clnu.2018.01.023
✅(در صورت جذابیت و علاقمندی به موضوع، مطلب را برای دیگران نیز بازنشر فرمایید).
📢کانال #دکترامیرمحمدشهسوارانی
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@DrAmirMohammadShahsavarani