Volume 35, Issue 6

In this article, we, for the first time, provide a comprehensive overview and unified framework of the impact of poverty and low socioeconomic status (SES) on the brain and behaviour. While there are many studies on the impact of low SES on the brain (including cortex, hippocampus, amygdala, and even neurotransmitters) and behaviours (including educational attainment, language development, development of psychopathological disorders), prior studies did not integrate behavioural, educational, and neural findings in one framework. Here, we argue that the impact of poverty and low SES on the brain and behaviour are interrelated. Specifically, based on prior studies, due to a lack of resources, poverty and low SES are associated with poor nutrition, high levels of stress in caregivers and their children, and exposure to socio-environmental hazards. These psychological and physical injuries impact the normal development of several brain areas and neurotransmitters. Impaired functioning of the amygdala can lead to the development of psychopathological disorders, while impaired hippocampus and cortex functions are associated with a delay in learning and language development as well as poor academic performance. This in turn perpetuates poverty in children, leading to a vicious cycle of poverty and psychological/physical impairments. In addition to providing economic aid to economically disadvantaged families, interventions should aim to tackle neural abnormalities caused by poverty and low SES in early childhood. Importantly, acknowledging brain abnormalities due to poverty in early childhood can help increase economic equity. In the current study, we provide a comprehensive list of future studies to help understand the impact of poverty on the brain.

Cognitive disorders such as major depressive disorder and bipolar disorder severely compromise brain function and neuronal activity. Treatments to restore cognitive abilities can have severe side effects due to their intense and excitatory nature, in addition to the fact that they are expensive and invasive. Low-field magnetic stimulation (LFMS) is a novel non-invasive proposed treatment for cognitive disorders. It repairs issues in the brain by altering deep cortical areas with treatments of low-intensity magnetic stimulation. This paper aims to summarize the current literature on the effects and results of LFMS in cognitive disorders. We developed a search strategy to identify relevant studies utilizing LFMS and systematically searched eight scientific databases. Our review suggests that LFMS could be a viable and effective treatment for multiple cognitive disorders, especially major depressive disorder. Additionally, longer, more frequent, and more personalized LFMS treatments tend to be more efficacious.

Peripheral nerve injury (PNI) is one of the most serious causes of disability and loss of work capacity of younger individuals. Although PNS has a certain degree of regeneration, there are still challenges like disordered growth, neuroma formation, and incomplete regeneration. Regarding the management of PNI, conventional methods such as surgery, pharmacotherapy, and rehabilitative therapy. Treatment strategies vary depending on the severity of the injury. While for the long nerve defect, autologous nerve grafting is commonly recognized as the preferred surgical approach. Nevertheless, due to lack of donor sources, neurological deficits and the low regeneration efficiency of grafted nerves, nerve guide conduits (NGCs) are recognized as a future promising technology in recent years. This review provides a comprehensive overview of current treatments for PNI, and discusses NGCs from different perspectives, such as material, design, fabrication process, and composite function.

While breathing is a vital, involuntary physiological function, the mode of respiration, particularly nasal breathing, exerts a profound influence on brain activity and cognitive processes. This review synthesizes existing research on the interactions between nasal respiration and the entrainment of oscillations across brain regions involved in cognition. The rhythmic activation of olfactory sensory neurons during nasal respiration is linked to oscillations in widespread brain regions, including the prefrontal cortex, entorhinal cortex, hippocampus, amygdala, and parietal cortex, as well as the piriform cortex. The phase-locking of neural oscillations to the respiratory cycle, through nasal breathing, enhances brain inter-regional communication and is associated with cognitive abilities like memory. Understanding the nasal breathing impact on brain networks offers opportunities to explore novel methods for targeting the olfactory pathway as a means to enhance emotional and cognitive functions.

Cerebral autoregulation is an intrinsic myogenic response of cerebral vasculature that allows for preservation of stable cerebral blood flow levels in response to changing systemic blood pressure. It is effective across a broad range of blood pressure levels through precapillary vasoconstriction and dilation. Autoregulation is difficult to directly measure and methods to indirectly ascertain cerebral autoregulation status inherently require certain assumptions. Patients with impaired cerebral autoregulation may be at risk of brain ischemia. One of the central mechanisms of ischemia in patients with metabolically compromised states is likely the triggering of spreading depolarization (SD) events and ultimately, terminal (or anoxic) depolarization. Cerebral autoregulation and SD are therefore linked when considering the risk of ischemia. In this scoping review, we will discuss the range of methods to measure cerebral autoregulation, their theoretical strengths and weaknesses, and the available clinical evidence to support their utility. We will then discuss the emerging link between impaired cerebral autoregulation and the occurrence of SD events. Such an approach offers the opportunity to better understand an individual patient’s physiology and provide targeted treatments.

This systematic review aimed to evaluate the effects of different theta burst stimulation (TBS) protocols on improving upper extremity motor functions in patients with stroke, their associated modulators of efficacy, and the underlying neural mechanisms. We conducted a meta-analytic review of 29 controlled trials published from January 1, 2000, to August 29, 2023, which investigated the effects of TBS on upper extremity motor, neurophysiological, and neuroimaging outcomes in poststroke patients. TBS significantly improved upper extremity motor impairment (Hedge’s g  = 0.646, p  = 0.003) and functional activity (Hedge’s g  = 0.500, p  < 0.001) compared to controls. Meta-regression revealed a significant relationship between the percentage of patients with subcortical stroke and the effect sizes of motor impairment ( p  = 0.015) and functional activity ( p  = 0.018). Subgroup analysis revealed a significant difference in the improvement of upper extremity motor impairment between studies using 600-pulse and 1200-pulse TBS ( p  = 0.002). Neurophysiological studies have consistently found that intermittent TBS increases ipsilesional corticomotor excitability. However, evidence to support the regional effects of continuous TBS, as well as the remote and network effects of TBS, is still mixed and relatively insufficient. In conclusion, TBS is effective in enhancing poststroke upper extremity motor function. Patients with preserved cortices may respond better to TBS. Novel TBS protocols with a higher dose may lead to superior efficacy compared with the conventional 600-pulse protocol. The mechanisms of poststroke recovery facilitated by TBS can be primarily attributed to the modulation of corticomotor excitability and is possibly caused by the recruitment of corticomotor networks connected to the ipsilesional motor cortex.

Overweight (OW) and obesity (OB) have become prevalent issues in the global public health arena. Serving as a prominent risk factor for various chronic diseases, overweight/obesity not only poses serious threats to people’s physical and mental health but also imposes significant medical and economic burdens on society as a whole. In recent years, there has been a growing focus on basic scientific research dedicated to seeking the neural evidence underlying overweight/obesity, aiming to elucidate its causes and effects by revealing functional alterations in brain networks. Among them, dysfunction in the reward network (RN) and executive control network (ECN) during both resting state and task conditions is considered pivotal in neuroscience research on overweight/obesity. Their aberrations contribute to explaining why persons with overweight/obesity exhibit heightened sensitivity to food rewards and eating disinhibition. This review centers on the reward and executive control network by analyzing and organizing the resting-state and task-based fMRI studies of functional brain network alterations in overweight/obesity. Building upon this foundation, the authors further summarize a reward-inhibition dual-system model, with a view to establishing a theoretical framework for future exploration in this field.