Brain-X最新文献

Traditional computing architectures based on complementary metal-oxide semiconductor technology suffer from von Neumann computing bottleneck,¹ resulting in poor computing efficiency and a huge energy consumption. To surpass the limits of conventional computation, scientists have begun to imitate the computational behavior of the human brain.² With the advantages of highly parallel computing, high error tolerance and low power consumption, the human brain and its neural systems have inspired the rapid development of novel neuromorphic computing hardware.³ There are ∼86 billion neurons in the biological neural system. Neurons can govern the membrane potential for associative learning, memory, and information processing, with important roles in brain-inspired neuromorphic computing. Therefore, constructing artificial neuron via electronic devices is key to the realization of neuronal dynamics in the human brain.

Different types of memristive neurons have been reported recently, such as phase-change memory, Mott insulators, magnetic memory, diffusive memristors and ferroelectric memory. The integrate-and-fire neuron function and spiking neural networks could be simulated based on the integration characteristic of these artificial neurons. Besides the characteristic of integration, nonlinearity is another necessary characteristic in neuronal emulation, especially for integrating the datastream during neuromorphic computing. However, the realization of nonlinear integration of excitatory and inhibitory postsynaptic potentials has not been reported in above artificial neurons. It is in urgent need to develop a novel artificial neuron with both nonlinear and integrated capabilities for high-efficiency computing.

The research team of Harish Bhaskaran proposed an atomically thin optomemristive feedback neuron using a stack of MoS₂, WS₂, and graphene (Figure 1).⁴ The heterojunction of MoS₂/WS₂ acts as a neural membrane, and the graphene acts as neural soma. Different from traditional artificial neurons, the proposed two-dimensional (2D) neuron device could exhibit a rectified-type of nonlinearity in its output characteristics without the need for additional circuitry and software. The 2D optomemristive neuron shows great potential in winner-take-all learning (WTA) computational tasks and unsupervised learning, which provide guidance for atomic-scale rectified and nonlinear optoelectronic neurons.

The key performance of device is based on the combination and broadcast of electrical excitatory signals and optical inhibitory signals, which could be used for nonlinear and rectified integration of information in neuromorphic computing. Under light illumination, electron-hole pairs could be induced and separated by the intrinsic field in transition metal dichalcogenides. The electrons transit from the het

Approximately 20% of cancer patients experience brain metastases in the advanced stages as circulating tumor cells migrate to and colonize the brain microvasculature. Due to the challenges associated with biopsies, our understanding of the tumor microenvironment and heterogeneity in brain metastases remains limited, hindering the development of systemic approaches for detection and treatment. Emerging evidence suggests that specific brain metastases induce a substantial level of immune activation and infiltration, which provides an opportunity to design specific immunotherapies targeting brain metastases. This perspective aims to summarize recent advancements in molecular profiling of the immune repertoires of brain metastases using biopsy-based approaches, with an emphasis on tumor-reactive T cells. Additionally, we discuss the potential of alternative tissues and technologies that offer improved temporal resolution, throughput, and fidelity for tracking tumor dynamics.

A growing body of evidence suggests that patients who experience traumatic brain injuries (TBIs) exhibit significantly shorter healing periods compared to those with isolated fractures. However, the precise underlying mechanism behind this phenomenon remains unclear. Recent studies have shed light on the potential role of hormonal signals and neural circuits originating in the hypothalamus, which play vital roles in regulating the skeletal system. Despite these advances, there is a lack of comprehensive research summarizing the crucial role of bone healing in TBIs and the underlying mechanisms. This review aimed to explore the underlying mechanisms responsible for the accelerated bone healing observed in TBI patients, with a specific focus on the intricate crosstalk between TBI and bone remodeling. Additionally, we comprehensively discuss and summarize the beneficial effects of TBI on the skeletal system and examine the TBI-induced signaling pathways that result in accelerated fracture healing and bone remodeling. By dissecting these pathways, we aim to identify potential targets for intervention and bone repair promotion.

Disabilities of the central nervous system (CNS), including chronic degeneration, threaten human life. Cell-based therapy is one of the promising treatment strategies, but obtaining enough functional neurons and surgically transplanting them represent major obstacles in clinical neuroscience. In recent years, cell reprogramming technology has broken the traditional understanding of cell biology and advanced rapidly. Adult cells can be reprogrammed into induced pluripotent stem cells (iPSCs) and converted into somatic cells from different lineages, such as induced neurons (iNs).

Direct neuronal reprogramming (dNR) is an emerging biotechnology with significant biomedical potential to produce functional iNs.¹ Methods to obtain functional neurons for adult CNS therapy are limited and rely mainly on stem cell differentiation. iPSC reprogramming, firstly reported in 2006, opened the door to obtaining embryonic stem cell (ESC)-like cells. Since then, protocols for direct cell reprogramming (transdifferentiation or conversion) have been widely tested due to the risk and cost of iPSCs. These methods force cells to change lineages from one to another without passing through the pluripotent state and have inspired a new understanding of biology and ushered in a new era in cell technology.

dNR is mainly based on the overexpression of various transcription factors (TFs). Different TF formulas, such as Ascl1/Brn2/Myt1L (converting human fibroblasts into dopaminergic iNs) and Sox2/Ascl1 (converting human pericytes into iNs) have been proposed in the laboratories. TFs such as Sox2 alter not only the transcriptome profile but also the chromatin structure; thus, they are heavily influential in cell reprogramming. On the other hand, biochemists performed dNR using small molecules (SMs). Mechanism studies showed that sequential treatment with various SMs can trigger various signal pathways, resulting in a boost in the reprogramming efficiency or direct generation of iNs. However, understanding in SM-triggered dNR is insufficient, such as the underlying biological mechanism, partial electrophysiological functions and production of neuron transmitters.

Epigenetic modulations, using biochemical and biophysical methods, have been observed during dNR. Fluctuations in the epigenetic state can induce a certain degree of cell identity disorder; thus, dNR can be triggered (so-called epigenetic reprogramming). Additional modulation of the chromatin and metabolism of the starter cells can enhance the efficiency of dNR. Through epigenetic modulation, biophysical forces, such as cell squeezing² and substrate topography,³ have been reported to facilitate dNR and regulate the ratios of iN subtypes. Advantages of using biophysical forces are that these stimulators are well defined and do not enter the cells. They generate unique mechanotransduction signalings through cytoskeletal and cell n

The human brain is one of the most complex and mysterious systems known to science. Despite the significant advances in neuroscience over the past few decades, our understanding of how the brain works remains limited. One of the key challenges in understanding brain function is determining its relationship with brain structure. However, a recent article published in Nature titled “Geometric Constraints on Human Brain Function” presents an innovative approach to understanding the complex interplay between brain structure and function.¹

The article argues that the physical architecture of the brain imposes geometric constraints on its function. Specifically, the authors propose that the arrangement and structure of neural connections play a vital role in determining the brain's functional capabilities. The article describes how the brain can be viewed as a network of interconnected nodes and edges, with the nodes representing neurons and the edges representing the connections between neurons.

The authors present several examples supporting this concept. They demonstrate how certain brain regions have higher degrees of connectivity, while others exhibit more localization of function. For instance, regions of the brain that are responsible for motor control have higher connectivity, while those that mediate sensory processing are more specialized.

The article also discusses how changes in connectivity due to disease or injury can lead to functional impairment. For example, an injury in the parietal cortex, which is involved in spatial awareness, can affect an individual's ability to navigate their surroundings. Similarly, changes in connectivity in the amygdala, which is involved in processing emotions, can cause mood disorders and anxiety.

Another interesting concept presented in the article is how the geometry of neural connections may be optimized for specific functions, such as object recognition or language processing. The authors propose that this optimization may be achieved through the connectivity of subnetworks with different geometries within the brain.

One of the strengths of the article is the use of mathematical models and simulations to test the proposed hypotheses. The authors developed a set of models that demonstrated how the geometry of neural connections affected brain function in different scenarios, such as the execution of motor tasks or the recognition of objects. These simulations provided evidence supporting the hypothesis that the brain's functional capabilities are determined, to some extent, by its physical geometry.

However, some limitations of the article should also be noted. First, the article relied heavily on mathematical modeling and simulation, which may not accurately reflect the complexity of the brain. Second, the study's focus on the physical structure of the brain may ignore the roles of other factors, such as genetic and environmental infl

As the integration of artificial intelligence (AI) into our daily lives and educational environments becomes increasingly prevalent, it is necessary to understand the way in which these technologies impact cognitive functions. AI models such as ChatGPT hold immense promise for advancing the field of education, making it easier than ever for educators to support personalized learning and for students to access information. However, there are risks associated with increased AI engagement; individuals may become over-reliant on AI, resulting in a reduced capacity for critical thinking, or a decline in memory retention. This article provides a comprehensive survey of these potential impacts, emphasizing the need for the judicious utilization of AI, and advocating for an integration approach that supplements, rather than supplants, human cognitive functions. The paper concludes by encouraging further research into the long-term cognitive effects of interacting with advanced AI models such as ChatGPT.

Hand function assessment is an essential component of the process of stroke rehabilitation because of the high incidence of hand motor dysfunction. In terms of the manual evaluation of hand function, the Fugl-Meyer scale is a recommended scale with high reliability and validity. However, the need for accurate assessments and increasing developments in technology has led to the promotion of automatic quantitative assessment systems for the hand. In this study, we collected quantitative data on hand function with an automatic system and the upper limb Fugl-Meyer assessment (FMA) from 79 people with stroke. We developed decision tree (DT) and gradient-boosted decision tree (GBDT) predictive models for the Fugl-Meyer score using features extracted from the Hand Automatic Quantitative Assessment System (HAQAS). Predictive performances were compared between these models regarding the predictive accuracy and Cohen's kappa. There were high correlations between features automatically collected by the HAQAS and the Fugl-Meyer scale in all the sub-items, with the maximal correlations all being over 0.5, indicating the high validity of the HAQAS in automatic FMA prediction. Hand functions were more highly correlated (average correlation coefficient 0.90) with HAQAS features than wrist functions (average correlation coefficient 0.54), and the GBDT achieved higher predictive accuracies and agreement than the DT algorithm. We conclude that the HAQAS is feasible for stroke patients with hand dysfunction and convenient for clinicians and therapists. This study was registered in the Chinese Clinical Trial Registry (ChiCTR1800019098).

Currently, no specific treatments are available for Alzheimer's disease (AD). Mild cognitive impairment (MCI), the preclinical stage of AD, has a high possibility of reversing symptoms through neural regulation. A state dynamics model for single brain regions was developed to simulate blood oxygen level-dependent signals in a patient with early mild cognitive impairment. Subsequently, the analysis of functional connections was used to comprehensively consider multiple complex network centralities to locate the intervention targets, and a multiple brain region collaborative control scheme was designed. Finally, the reliability and effectiveness of the intervention were verified at the brain region and subnetwork levels. This technique provides a basis for future clinical diagnosis and treatment of AD and MCI.

Acute myocardial infarction (AMI) occurs in 1.6%–2.1% of patients with acute stroke.¹ Primary percutaneous coronary intervention (PCI) and antithrombotic therapy, which improve cardiovascular outcomes in patients with AMI, may elevate the risks of hemorrhagic stroke in the acute phase of stroke.² How to manage the ischemic and bleeding risks in patients with AMI complicating acute stroke (AMI-CAS) is challenging in clinics. Therapeutics for AMI-CAS should be well-balanced by collaborating with cardiologists and neurologists. The institute in the present study has a structure to provide a heart–brain team approach,³ which was defined as cardiac catheterization and antithrombotic therapies, according to the status and severity of an acute stroke and the patient's condition.

In this issue of the Journal of the American Heart Association, Suzuki et al.⁴ described different clinical characteristics, coronary revascularization and antithrombotic therapies and cardiovascular and major bleeding outcomes of patients with AMI-CAS. These findings were based on a retrospective cohort study using data from the National Cerebral and Cardiovascular Center (Suita, Japan) between 1 January 2007, and 30 September 2020 and included 2393 consecutive patients with AMI. Of these patients, those with takotsubo cardiomyopathy (n = 3) were excluded. The primary outcome was defined as a composite of major adverse cerebral/cardiovascular events (MACCEs), which included cardiac-cause death, nonfatal myocardial infarction, and nonfatal stroke. The authors reported a few attractive findings. Firstly, AMI-CAS was identified in 1.6% (39/2390) of study participants in the current study. The characteristics of AMI-CAS tend to be women (46.2% vs. 26.2%; P = 0.005), chronic kidney disease (71.8% vs. 47.0%; P = 0.002), atrial fibrillation (38.5% vs. 9.8%; P < 0.001) and stroke (33.3% vs. 11.1%; P < 0.001). In 39 patients with AMI-CAS, 37 patients (37/39 = 94.9%) and 2 patients (2/39 = 5.1%) were diagnosed as having an ischemic stroke or hemorrhagic stroke, respectively. 69.2% and 10.3% of them were attributable to cardioembolic and atherosclerotic causes, respectively. AMI occurred within 3 days from the onset of acute stroke in 59.0% of patients with AMI-CAS, and the median duration of AMI from the onset of acute stroke was 2 days (interquartile range, 0–8 days). Secondly, medical procedures were conducted with a diverse frequency between AMI-CAS patients and AMI patients without acute stroke. Primary PCI (43.6% vs. 84.7%; p < 0.001), stent implantation (30.8% vs. 77.9%; p < 0.001) and dual-antithrombotic therapy (38.5% vs. 85.7%) were less frequently received in AMI-CAS, whereas thrombectomy (7.7% vs. 1.4%; p = 0.02) was higher than AMI patients without acute stroke. Additionally, angiotensin-converting

Alzheimer's disease (AD) is the most common neurodegenerative disorder worldwide. Because of the complex pathogenesis of AD and the unique location of AD lesions, effective clinical treatment strategies for this disease remain elusive. However, the development of nanotechnology has allowed a new era of AD treatment to emerge. AD nanomedicines are products of interdisciplinary research that enable high precision and targeted delivery. Additionally, they can specifically regulate various pathogenic factors. This review focuses on nanomedicines based on the pathological mechanisms of AD that can target AD lesions. We also discuss the precise regulatory effects of nanomedicines (including the nanomaterials themselves) on pathogenic proteins, neuroinflammatory molecules, and other pathogenic factors. We summarize the clinical trials that have examined new AD drugs, highlighting the development of new nanomedicines and the progress in their clinical translation. Nanotechnology-based AD treatment is a nascent field, and a complete cure is distant at present; therefore, we also elaborate on the shortcomings of current AD nanomedicines. Finally, we discuss the prospects to guide the future development of AD nanomedicines.