Reviews in the Neurosciences最新文献

{"title":"Antimicrobial peptides and proteins in Alzheimer's and Parkinson's diseases: implications for biomarker exploration.","authors":"Shin Jie Yong, Seong Lin Teoh, Ishwar S Parhar, Tomoko Soga, Wei Ling Lim, Jactty Chew","doi":"10.1515/revneuro-2025-0034","DOIUrl":"https://doi.org/10.1515/revneuro-2025-0034","url":null,"abstract":"<p><p>Biomarkers are necessary tools to validate the diagnosis of Alzheimer's and Parkinson's diseases (AD and PD), especially when clinical symptoms are less apparent in the early stages of diseases. Current biomarkers used in clinical practice rely on brain imaging and cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) peptides and α-synuclein (α-syn) for AD and PD, respectively. However, these diagnostic techniques are not only highly invasive and costly, but they also face limitations in diagnostic accuracy, particularly for preclinical or early stages of diseases. Thus, alternative biomarkers have been sought, preferably those in more accessible and convenient biofluids. Given that antimicrobial peptides and proteins (AMPs) may interact with the neuropathogenesis of AD and PD, AMPs have been recognized as promising candidate biomarkers for AD and PD. Therefore, this review examines the literature on how levels of certain AMPs (lactoferrin, hepcidin, defensin, dermcidin, histatin, cathelicidin L-37, prion protein, amylin or islet amyloid polypeptide, substance P or neurokinin-1, and neuropeptide Y) change in the CSF and more accessible biofluids (serum, plasma, tear, or saliva) in AD and PD patients compared to controls. Based on these findings, this review highlights the advantages, challenges, and future directions of AMP-based biomarkers for AD and PD.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144295222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From genetic roots to recent advancements in gene therapy targeting amyloid beta in Alzheimer's disease.","authors":"Pinar Peyvand, Pantea Allami, Nima Rezaei","doi":"10.1515/revneuro-2025-0025","DOIUrl":"https://doi.org/10.1515/revneuro-2025-0025","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is one of the most prevalent neurodegenerative disorders. The pathological hallmarks of AD are amyloid-beta (Aβ) plaques and tau protein tangles, which cause neurodegeneration and lead to cognitive decline. The distinguished role of Aβ plaques in the onset of the disease, especially in familial AD, alongside the genetic complexity of AD, underscores the need for precise and targeted genetic interventions targeting Aβ. This review first highlights the amyloidogenic and non-amyloidogenic pathways and inflammatory mechanisms contributing to Aβ accumulation. It also introduces the role of genetic variants such as <i>amyloid precursor protein (APP), presenilin (PSEN1), PSEN2, and Apolipoprotein E (APOE)</i> alongside the molecular and cellular mechanisms involved in Aβ pathology. Then, gene therapy techniques are discussed for their potential to target Aβ either directly by inhibiting its production or enhancing its degradation or indirectly by targeting APOE, inflammatory pathways, and neurotrophic factors. While these approaches show significant preclinical promise, challenges such as timing, safety, and delivery across the blood-brain barrier persist and need further investigation.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The current approaches to modeling the brain ischemia-reperfusion and inflammation: from animal models toward vascularized and neuroimmune cerebral organoids.","authors":"Pavel P Tregub, Daria D Volegova, Arseniy K Berdnikov, Pavel A Chekulaev, Daniil A Bystrov, Yulia K Komleva, Natalia A Kolotyeva, Sergey N Illarioshkin, Alla B Salmina, Stanislav O Yurchenko","doi":"10.1515/revneuro-2025-0015","DOIUrl":"https://doi.org/10.1515/revneuro-2025-0015","url":null,"abstract":"<p><p>For several decades, the modeling of brain diseases in experimental animals has remained one of the key components of studying the pathogenesis of central nervous system pathology and searching for new methods of prevention and therapy. In recent years, new approaches to modeling pathological conditions <i>in vitro</i> have been in active development; these approaches will not only reduce the number of animal studies but also allow us to take a step toward reproducing the human-specific mechanisms of brain pathology. In this review, we characterize the most common rodent models of cerebral ischemia and reperfusion, as well as neuroinflammation inherent to neurodegeneration (in particular, Parkinson's disease), which are reproduced <i>in vivo</i>. This review addresses engineering and technical challenges and the prospects for the development of brain pathology models <i>in vitro</i>, e.g., vascularized and microglia-containing/neuroimmune cerebral organoids, which may be useful in overcoming the shortcomings and limitations of the current <i>in vivo</i> models.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144182885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise-induced modulation of miRNAs and gut microbiome: a holistic approach to neuroprotection in Alzheimer's disease.","authors":"Rui Wang, Juan Li, Xiaochen Li, Yan Guo, Pei Chen, Tian Peng","doi":"10.1515/revneuro-2025-0013","DOIUrl":"https://doi.org/10.1515/revneuro-2025-0013","url":null,"abstract":"<p><p>Alzheimer's disease (AD), a progressive neurodegenerative disorder, is marked by cognitive decline, neuroinflammation, and neuronal loss. MicroRNAs (miRNAs) have emerged as critical regulators of gene expression, influencing key pathways involved in neuroinflammation and neurodegeneration in AD. This review delves into the multifaceted role of exercise in modulating miRNA expression and its interplay with the gut microbiome, proposing a comprehensive framework for neuroprotection in AD. By synthesizing current research, we elucidate how exercise-induced changes in miRNA profiles can mitigate inflammatory responses, promote neurogenesis, and reduce amyloid-beta and tau pathologies. Additionally, we explore the gut-brain axis, highlighting how exercise-driven alterations in gut microbiota composition can further influence miRNA expression, thereby enhancing cognitive function and reducing neuroinflammatory markers. This holistic approach underscores the potential of targeting exercise-regulated miRNAs and gut microbiome interactions as a novel, noninvasive therapeutic strategy to decelerate AD progression and improve quality of life for patients. This approach aims to decelerate disease progression and improve patient outcomes, offering a promising avenue for enhancing the effectiveness of AD management.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A proposed role for electrical coupling in the neocortical slow oscillation.","authors":"Roger D Traub, Andreas Draguhn, Diego Contreras, Mark O Cunningham","doi":"10.1515/revneuro-2025-0018","DOIUrl":"https://doi.org/10.1515/revneuro-2025-0018","url":null,"abstract":"<p><p>We constructed a computational thalamocortical network model for study of the neocortical slow oscillation. It incorporated a number of neuronal types, both excitatory and inhibitory, each model neuron simulated as a multicompartment entity with numerous membrane conductances. As in previous experimental and modeling studies, simulated slow oscillations primarily depended on recurrently connected deep intrinsic bursting (IB) pyramidal cells, with NMDA receptors being critical as well as intrinsic membrane conductances (e.g. persistent Na⁺); and with repolarization to the Down state dependent on intrinsic (slow Ca²⁺-dependent K⁺) and synaptic (GABA_B receptor mediated) conductances. Furthermore, however, we now can account for additional features of the slow oscillation: the frequent occurrence of spikelets, the presence of very fast ripple-like oscillations, and the transition to so-called fast runs (10 to ∼20 Hz bursty oscillations). These latter phenomena depended in our model on electrical coupling via gap junctions between pyramidal neurons. The importance of gap junctions is supported by previous experimental data on the ripple-blocking effect of halothane, as well as by data from the <i>in vitro</i> hippocampus.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gamma oscillations as correlates of depression: updating Fitzgerald and Watson (2018).","authors":"Sarah L Coleman, Christopher F Sharpley, Kirstan A Vessey, Ian D Evans, Rebecca J Williams, Vicki Bitsika","doi":"10.1515/revneuro-2025-0023","DOIUrl":"https://doi.org/10.1515/revneuro-2025-0023","url":null,"abstract":"<p><p>Depression remains one of the most common and debilitating neuropsychiatric conditions, with little consistency in treatment efficacy. Some of the lack of success in developing effective treatments has been the absence of a reliable biomarker of depression, despite many attempts. One such potential biomarker is the electrical activity of the brain that occurs in the gamma band (30-200 Hz). To evaluate the state of research into gamma as a biomarker of depression, a review of recent research literature was conducted. A total of 31 relevant papers was identified, 22 of which used resting-state studies, and nine included a stimulus-task. These studies were examined here in terms of their definition of gamma, sample sizes, research focus, brain region examined, and EEG methodologies used. Due to the range of methodologies, some inconsistent results emerged but several valuable findings remained, including that depressed patients usually had higher gamma power than their healthy controls (HC), that the imposition of a perceptual task into the research protocol also introduced a strong element of confound to the results, and that studies that sought to evaluate the role of gamma in treatment were yet to be established as reliable. Key issues for future research are discussed, and the potential for gamma as a biomarker of depression is evaluated as emerging.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143994935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of glutamate receptors and transporters in epilepsy: evidence from animal studies.","authors":"Jéssica Alves Lemes, Barbara Dos Anjos Rosário, Sophia Morya Santos Rocha, Susana Sieiro Bandeira, Alessandra Mussi Ribeiro, Sandra Henriques Vaz, Ana Maria Sebastião, Adam Armada-Moreira, Daniel Araki Ribeiro, Milena de Barros Viana","doi":"10.1515/revneuro-2024-0173","DOIUrl":"https://doi.org/10.1515/revneuro-2024-0173","url":null,"abstract":"<p><p>Epilepsy encompasses a group of chronic brain disorders characterized by recurrent, hypersynchronous activity of neuronal clusters, with epileptic seizures being the primary manifestation of these disorders. The objective of epilepsy treatment is to prevent seizures with minimum adverse side effects. However, approximately 30 % of patients do not respond to available medications. One proposed mechanism of epileptogenesis is glutamate excitotoxicity. When released in excess or not appropriately removed from the synaptic cleft, glutamate hyperactivates receptors, causing a biochemical cascade, which culminates in seizures and cell death. The use of animal models is essential for uncovering potential epileptogenic pathways, understanding the role of receptors and transporters in excitotoxicity, and screening effective antiepileptic treatments. This review examines studies that investigate the role of glutamate transporters and receptors in excitotoxicity and epileptogenesis using animal models. For this, we searched through both PubMed/Medline and ScienceDirect databases. After applying the inclusion and exclusion criteria, 26 (twenty-six) studies were selected for analysis. The studies addressed key glutamate transporter family of excitatory amino acid transporters (EAATs) EAAT1, EAAT2, and EAAT3, responsible for glutamate clearance, as well as AMPA receptor subunits GluA1 and GluA2, NMDA receptor subunits GluN1, GluN2a, and GluN2b, and the metabotropic receptors mGluR5 and mGluR2/3. Results showed that the dysregulation of these transporters and receptors is associated to seizure induction and excitotoxic damage, pointing to their fundamental role in the mechanisms of excitotoxicity and epileptogenesis. These findings highlight the potential of targeting glutamate transporters and receptors to stabilize glutamate homeostasis as an intervention in epilepsy management.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroinflammation in diabetic peripheral neuropathy and therapeutic implications.","authors":"Zhao Zhong Chong, Nizar Souayah","doi":"10.1515/revneuro-2025-0031","DOIUrl":"https://doi.org/10.1515/revneuro-2025-0031","url":null,"abstract":"<p><p>Diabetic peripheral neuropathy (DPN) is a serious complication of diabetes mellitus, which is a common cause of disability in individuals with diabetes mellitus. Multiple mechanisms may be involved in the development of DPN. Neuroinflammation is a critical factor contributing to nerve damage during diabetes. Inflammation can induce the development of diabetes mellitus, and long-term hyperglycemia also causes increased oxidative stress and promotes the release of inflammatory cytokines. After reading through the literature, the association of inflammation with the induction of diabetes and DPN was discussed in the review. Inflammation induces nerve damage and nerve conduction impairment. The neuropathic pain in diabetes-induced DPN is also closely associated with the inflammatory response. Given the important roles of inflammation in diabetes-induced DPN, explicit elucidation of neuroinflammation during diabetes mellitus and DPN should hold the potential for developing novel therapeutic strategies for DPN. Experimental studies and limited clinical trials support the value of anti-inflammatory reagents in treating DPN, and the positive outcomes of these investigations warrant further clinical trials.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tryptophan metabolism in migraine: a review of experimental and clinical studies and a need to enhance research strategies.","authors":"Michal Fila, Jan Chojnacki, Marcin Derwich, Cezary Chojnacki, Elzbieta Pawlowska, Janusz Blasiak","doi":"10.1515/revneuro-2025-0008","DOIUrl":"https://doi.org/10.1515/revneuro-2025-0008","url":null,"abstract":"<p><p>Tryptophan (TRP) metabolism produces various neuroactive substances in the gastrointestinal tract, as well as in the central and peripheral nervous systems and intestinal microbiota. Initially centered on the serotonin pathway in TRP metabolism and TRP itself, many studies are now focusing on the kynurenine pathway, with an increasing interest in the indole pathway. Several TRP metabolites have been associated with migraines, suggesting that TRP metabolism may serve as a potential therapeutic target. However, these studies have significant limitations, including a small number of participants, a lack of standardized diets prior to and/or during clinical trials, and insufficient information regarding the transformation of TRP after its intake. Furthermore, no thorough study encompasses all the essential components of TRP metabolism: products, enzymes, receptors, and transporters. Different mechanisms may explain the involvement of TRP metabolism in migraines, including glutamate signaling and neurovasodilatory, immune, oxidative, and inflammatory processes. The results of studies on the role of TRP metabolism in migraine may be helpful for making dietary recommendations for migraine prevention and clinical management; however, individual characteristics for metabolizing TRP should be considered. The aim of this narrative perspective review is to critically present the results of studies on the role of TRP metabolism in migraine and explore their implications for migraine prevention and therapy. Unlike many other reviews that focus solely on either the serotonin or kynurenine pathway, our paper addresses all three primary TRP metabolism pathways.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From postsynaptic neurons to astrocytes: the link between glutamate metabolism, Alzheimer's disease and Parkinson's disease.","authors":"Fu-Wang Liu, Xue-Rui Zhang, Yi-Fan Cong, Yan-Man Liu, Han-Ting Zhang, Xue-Qin Hou","doi":"10.1515/revneuro-2024-0143","DOIUrl":"https://doi.org/10.1515/revneuro-2024-0143","url":null,"abstract":"<p><p>Glutamate is not only the main excitatory neurotransmitter of the human central nervous system, but also a potent neurotoxin. Therefore, maintaining low-dose, non-toxic extracellular glutamate concentrations between synapses to ensure the reliability of synaptic transmission is essential for maintaining normal physiological functions of neurons. More and more studies have confirmed that the specific pathogenesis of central nervous system diseases (such as Alzheimer's disease) caused by neuronal damage or death due to abnormal inter-synaptic glutamate concentration may be related to the abnormal function of excitatory amino acid transporter proteins and glutamine synthetase on astrocytes, and that the abnormal expression and function of the above two proteins may be related to the transcription, translation, and even modification of both by the process of transcription, translation, and even modification of astrocytes. oxidative stress, and inflammatory responses occurring in astrocytes during their transcription, translation and even modification. Therefore, in this review, we mainly discuss the relationship between glutamate metabolism (from postsynaptic neurons to astrocytes), Alzheimer's disease and Parkinson's disease in recent years.</p>","PeriodicalId":49623,"journal":{"name":"Reviews in the Neurosciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}