Volume 34, Issue 8

There has been tremendous progress in artificial neural networks (ANNs) over the past decade; however, the gap between ANNs and the biological brain as a learning device remains large. With the goal of closing this gap, this paper reviews learning mechanisms in the brain by focusing on three important issues in ANN research: efficiency, continuity, and generalization. We first discuss the method by which the brain utilizes a variety of self-organizing mechanisms to maximize learning efficiency, with a focus on the role of spontaneous activity of the brain in shaping synaptic connections to facilitate spatiotemporal learning and numerical processing. Then, we examined the neuronal mechanisms that enable lifelong continual learning, with a focus on memory replay during sleep and its implementation in brain-inspired ANNs. Finally, we explored the method by which the brain generalizes learned knowledge in new situations, particularly from the mathematical generalization perspective of topology. Besides a systematic comparison in learning mechanisms between the brain and ANNs, we propose “Mental Schema 2.0,” a new computational property underlying the brain’s unique learning ability that can be implemented in ANNs.

Guillain–Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy; a disease involving the peripheral nervous system which is the most common cause of acute flaccid paralysis worldwide. So far, it is still lack of a comprehensive overview and understanding of the national epidemiological, clinical characteristics, and the risk factors of GBS in China, as well as differences between China and other countries and regions in these respects. With the global outbreak of the coronavirus disease 2019 (COVID-19), an epidemiological or phenotypic association between severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and GBS has attracted great attention. In this review, we outlined the current clinical data of GBS in China by retrieving literature, extracting and synthesizing the data of GBS in China from 2010 to 2021. Besides, we compared the characteristics of epidemiology, preceding events and clinical profiles of GBS between China and other countries and regions. Furthermore, in addition to conventional intravenous immunoglobulin (IVIG) and plasma exchange (PE) therapy, the potential therapeutic effects with novel medications in GBS, such as complement inhibitors, etc., have become the research focus in treatments. We found that epidemiological and clinical findings of GBS in China are approximately consistent with those in the International GBS Outcome Study (IGOS) cohort. We provided an overall picture of the present clinical status of GBS in China and summarized the global research progress of GBS, aiming to further understand the characteristics of GBS and improve the future work of GBS worldwide, especially in countries with the middle and low incomes.

Pain is a multifaceted process that encompasses unpleasant sensory and emotional experiences. The essence of the pain process is aversion, or perceived negative emotion. Central sensitization plays a significant role in initiating and perpetuating of chronic pain. Melzack proposed the concept of the “pain matrix”, in which brain regions associated with pain form an interconnected network, rather than being controlled by a singular brain region. This review aims to investigate distinct brain regions involved in pain and their interconnections. In addition, it also sheds light on the reciprocal connectivity between the ascending and descending pathways that participate in pain modulation. We review the involvement of various brain areas during pain and focus on understanding the connections among them, which can contribute to a better understanding of pain mechanisms and provide opportunities for further research on therapies for improved pain management.

The transsulfuration pathway (TSP) is a metabolic pathway involving sulfur transfer from homocysteine to cysteine. Transsulfuration pathway leads to many sulfur metabolites, principally glutathione, H 2 S, taurine, and cysteine. Key enzymes of the TSP, such as cystathionine β-synthase and cystathionine γ-lyase, are essential regulators at multiple levels in this pathway. TSP metabolites are implicated in many physiological processes in the central nervous system and other tissues. TSP is important in controlling sulfur balance and optimal cellular functions such as glutathione synthesis. Alterations in the TSP and related pathways (transmethylation and remethylation) are altered in several neurodegenerative diseases, including Parkinson’s disease, suggesting their participation in the pathophysiology and progression of these diseases. In Parkinson’s disease many cellular processes are comprised mainly those that regulate redox homeostasis, inflammation, reticulum endoplasmic stress, mitochondrial function, oxidative stress, and sulfur content metabolites of TSP are involved in these damage processes. Current research on the transsulfuration pathway in Parkinson’s disease has primarily focused on the synthesis and function of certain metabolites, particularly glutathione. However, our understanding of the regulation of other metabolites of the transsulfuration pathway, as well as their relationships with other metabolites, and their synthesis regulation in Parkinson´s disease remain limited. Thus, this paper highlights the importance of studying the molecular dynamics in different metabolites and enzymes that affect the transsulfuration in Parkinson’s disease.

In recent decade microglia have been found to have a central role in the development of chronic neuropathic pain after injury to the peripheral nervous system. It is widely accepted that peripheral nerve injury triggers microglial activation in the spinal cord, which contributes to heightened pain sensation and eventually chronic pain states. The contribution of microglia to chronic pain arising after injury to the central nervous system, such as spinal cord injury (SCI), has been less studied, but there is evidence supporting microglial contribution to central neuropathic pain. In this systematic review, we focused on post-SCI microglial activation and how it is linked to emergence and maintenance of chronic neuropathic pain arising after SCI. We found that the number of studies using animal SCI models addressing microglial activity is still small, compared with the ones using peripheral nerve injury models. We have collected 20 studies for full inclusion in this review. Many mechanisms and cellular interactions are yet to be fully understood, although several studies report an increase of density and activity of microglia in the spinal cord, both in the vicinity of the injury and in the spared spinal tissue, as well as in the brain. Changes in microglial activity come with several molecular changes, including expression of receptors and activation of signalling pathways. As with peripheral neuropathic pain, microglia seem to be important players and might become a therapeutic target in the future.