Reviews in the Neurosciences最新文献

Down syndrome (DS), a genetic pathology caused by triplication of chromosome 21, is characterized by brain hypotrophy and impairment of cognition starting from infancy. While studies in mouse models of DS have elucidated the major neuroanatomical and neurochemical defects of DS, comparatively fewer investigations have focused on the electrophysiology of the DS brain. Electrical activity is at the basis of brain functioning. Therefore, knowledge of the way in which brain circuits operate in DS is fundamental to understand the causes of behavioral impairment and devise targeted interventions. This review summarizes the state of the art regarding the electrical properties of the DS brain, starting from individual neurons and culminating in signal processing in whole neuronal networks. The reported evidence derives from mouse models of DS and from brain tissues and neurons derived from individuals with DS. EEG data recorded in individuals with DS are also provided as a key tool to understand the impact of brain circuit alterations on global brain activity.

The mechanisms governing neurological and functional recovery after ischemic stroke are incompletely understood. Recent advances in knowledge of intrinsic repair processes of the CNS have so far translated into minimal improvement in outcomes for stroke victims. Better understanding of the processes underlying neurological recovery after stroke is necessary for development of novel therapeutic approaches. Angiogenesis and neurogenesis have emerged as central mechanisms of post-stroke recovery and potential targets for therapeutics. Frameworks have been developed for conceptualizing cerebral angiogenesis and neurogenesis at the tissue and cellular levels. These models highlight that angiogenesis and neurogenesis are linked to each other and to functional recovery. However, knowledge of the molecular framework linking angiogenesis and neurogenesis after stroke is limited. Studies of potential therapeutics typically focus on one mediator or pathway with minimal discussion of its role within these multifaceted biochemical processes. In this article, we briefly review the current understanding of the coupled processes of angiogenesis and neurogenesis after stroke. We then identify the molecular mediators and signaling pathways found in pre-clinical studies to upregulate both processes after stroke and contextualizes them within the current framework. This report thus contributes to a more-unified understanding of the molecular mediators governing angiogenesis and neurogenesis after stroke, which we hope will help guide the development of novel therapeutic approaches for stroke survivors.

Extensive human studies and animal models show that chronic immune system stimulation involving microglia, inflammasome, complement activation, synthesis of cytokines, and reactive oxygen species exacerbates neurodegeneration in Alzheimer's disease (AD) and other tauopathies. Abnormalities in tau, Aβ, and microglial activation are frequently observed in dementia patients and indicate that these elements may work in concert to cause cognitive impairment. Contradicting reports from postmortem studies demonstrating the presence of Aβ aggregates in the brains of cognitively healthy individuals, as well as other investigations, show that tau aggregation is more strongly associated with synapse loss, neurodegeneration, and cognitive decline than amyloid pathology. Tau association with microtubules' surface promotes their growth and maintains their assembly, dynamicity, and stability. In contrast, the reduced affinity of hyperphosphorylated and mislocalized tau to microtubules leads to axonal deficits and neurofibrillary tangles (NFTs). Loss of microglial neuroprotective and phagocytic functions, as indicated by the faulty clearance of amyloid plaques, as well as correlations between microglial activation and tau tangle spread, all demonstrate the critical involvement of malfunctioning microglia in driving tau propagation. This review discusses the recent reports on the contribution of microglial cells to the development and progression of tau pathology. The detailed study of pathogenic mechanisms involved in interactions between neuroinflammation and tau spread is critical in identifying the targets for efficacious treatment strategies in AD.

This systematic review examines the effect of photobiomodulation (PBM), the application of red to near infrared light on body tissues, on the neuroinflammatory response and oxidative stress in animal models of neurodegenerative diseases. The research question and search protocol were prospectively registered on the PROSPERO database. Neurodegenerative diseases are becoming ever more prevalent in the ageing populations across the Western world, with no disease-modifying or neuroprotective treatment options being available. Hence there is a real need for the development of effective treatment options for patients. Inflammatory responses and oxidative stress within the central nervous system have a strong correlation with neuronal cell death. PBM is a non-invasive therapeutic option that has shown efficacy and promising effects in animal models of neurodegenerative disease; many studies have reported neuroprotection and improved behavioural outcomes. To the best of our knowledge, there has been no previous study that has reviewed the anti-inflammatory and the antioxidant effect of PBM in the context of neurodegeneration. This review has examined this relationship in animal models of a range of neurodegenerative diseases. We found that PBM can effectively reduce glial activation, pro-inflammatory cytokine expression and oxidative stress, whilst increasing anti-inflammatory glial responses and cytokines, and antioxidant capacity. These positive outcomes accompanied the neuroprotection evident after PBM treatment. Our review provides further indication that PBM can be developed into an effective non-pharmacological intervention for neurodegenerative diseases.

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.

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.

In recent years, the role of mitochondrial dynamics in neurodegenerative diseases has becoming increasingly important. More and more evidences have shown that in pathological conditions, abnormal mitochondrial divisions, especially Drp1-Fis1-mediated divisions, play an important role in the occurrence and development of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, glaucoma, and other neurodegenerative diseases. This review highlights several new mechanisms of physiological fission of mitochondria and the difference/connection of physiological/pathological mitochondrial fission. In addition, we described the relationship between abnormal mitochondrial dynamics and neurodegenerative diseases in detail and emphatically summarized its detection indicators in basic experiments, trying to provide references for further mechanism exploration and therapeutic targets.

Current literature lacks consolidated evidence for the impact of stimulation parameters on the effects of transcranial direct current stimulation (tDCS) in enhancing upper limb motor learning. Hence, we aim to synthesise available methodologies and results to guide future research on the usage of tDCS on upper limb motor learning, specifically in older adults and Parkinson's disease (PD). Thirty-two studies (Healthy older adults, N = 526, M = 67.25, SD = 4.30 years; PD, N = 216, M = 66.62, SD = 6.25 years) were included in the meta-analysis. All included studies consisted of active and sham protocols. Random effect meta-analyses were conducted for (i) subjects (healthy older adults and PD); (ii) intensity (1.0, 1.5, 2 mA); (iii) electrode montage (unilateral anodal, bilateral anodal, unilateral cathodal); (iv) stimulation site (cerebellum, frontal, motor, premotor, SMA, somatosensory); (v) protocol (online, offline). Significant tDCS effect on motor learning was reported for both populations, intensity 1.0 and 2.0 mA, unilateral anodal and cathodal stimulation, stimulation site of the motor and premotor cortex, and both online and offline protocols. Regression showed no significant relationship between tDCS effects and density. The efficacy of tDCS is also not affected by the number of sessions. However, studies that reported only single session tDCS found significant negative association between duration with motor learning outcomes. Our findings suggest that different stimulation parameters enhanced upper limb motor learning in older adults and PD. Future research should combine tDCS with neuroimaging techniques to help with optimisation of the stimulation parameters, considering the type of task and population.

Neuroplasticity or neural plasticity implicates the adaptive potential of the brain in response to extrinsic and intrinsic stimuli. The concept has been utilized in different contexts such as injury and neurological disease. Neuroplasticity mechanisms have been classified into neuroregenerative and function-restoring processes. In the context of injury, neuroplasticity has been defined in three post-injury epochs. Testosterone plays a key yet double-edged role in the regulation of several neuroplasticity alterations. Research has shown that testosterone levels are affected by numerous factors such as age, stress, surgical procedures on gonads, and pharmacological treatments. There is an ongoing debate for testosterone replacement therapy (TRT) in aging men; however, TRT is more useful in young individuals with testosterone deficit and more specific subgroups with cognitive dysfunction. Therefore, it is important to pay early attention to testosterone profile and precisely uncover its harms and benefits. In the present review, we discuss the influence of environmental factors, aging, and gender on testosterone-associated alterations in neuroplasticity, as well as the two-sided actions of testosterone in the nervous system. Finally, we provide practical insights for further study of pharmacological treatments for hormonal disorders focusing on restoring neuroplasticity.