{"title":"Subscription and Copyright Information","authors":"","doi":"10.1016/s0166-2236(24)00107-3","DOIUrl":"https://doi.org/10.1016/s0166-2236(24)00107-3","url":null,"abstract":"No Abstract","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":"26 1","pages":""},"PeriodicalIF":15.9,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141571241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in NeurosciencesPub Date : 2024-07-01Epub Date: 2024-05-27DOI: 10.1016/j.tins.2024.05.004
Amanda L Woerman, Jason C Bartz
{"title":"Effect of host and strain factors on α-synuclein prion pathogenesis.","authors":"Amanda L Woerman, Jason C Bartz","doi":"10.1016/j.tins.2024.05.004","DOIUrl":"10.1016/j.tins.2024.05.004","url":null,"abstract":"<p><p>Prion diseases are a group of neurodegenerative disorders caused by misfolding of proteins into pathogenic conformations that self-template to spread disease. Although this mechanism is largely associated with the prion protein (PrP) in classical prion diseases, a growing literature indicates that other proteins, including α-synuclein, rely on a similar disease mechanism. Notably, α-synuclein misfolds into distinct conformations, or strains, that cause discrete clinical disorders including multiple system atrophy (MSA) and Parkinson's disease (PD). Because the recognized similarities between PrP and α-synuclein are increasing, this review article draws from research on PrP to identify the host and strain factors that impact disease pathogenesis, predominantly in rodent models, and focuses on key considerations for future research on α-synuclein prions.</p>","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":" ","pages":"538-550"},"PeriodicalIF":14.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11236502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in NeurosciencesPub Date : 2024-07-01Epub Date: 2024-06-10DOI: 10.1016/j.tins.2024.05.005
Nagendran Ramalingam, Christian Haass, Ulf Dettmer
{"title":"Physiological roles of α-synuclein serine-129 phosphorylation - not an oxymoron.","authors":"Nagendran Ramalingam, Christian Haass, Ulf Dettmer","doi":"10.1016/j.tins.2024.05.005","DOIUrl":"10.1016/j.tins.2024.05.005","url":null,"abstract":"<p><p>α-Synuclein (αS) is an abundant presynaptic protein that regulates neurotransmission. It is also a key protein implicated in a broad class of neurodegenerative disorders termed synucleinopathies, including Parkinson's disease (PD) and Lewy body dementia (LBD). Pathological αS deposits in these diseases, Lewy bodies (LBs)/neurites (LNs), contain about 90% of αS in its phospho-serine129 (pS129) form. Therefore, pS129 is widely used as a surrogate marker of pathology. However, recent findings demonstrate that pS129 is also physiologically triggered by neuronal activity to positively regulate synaptic transmission. In this opinion article, we contrast the literature on pathological and physiological pS129, with a special focus on the latter. We emphasize that pS129 is ambiguous and knowledge about the context is necessary to correctly interpret changes in pS129.</p>","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":" ","pages":"480-490"},"PeriodicalIF":14.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141306918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in NeurosciencesPub Date : 2024-07-01Epub Date: 2024-05-17DOI: 10.1016/j.tins.2024.05.003
Aaron Keith West, Eve Rebecca Schneider
{"title":"A novel suppressor of Piezo2 in rodent nociceptors.","authors":"Aaron Keith West, Eve Rebecca Schneider","doi":"10.1016/j.tins.2024.05.003","DOIUrl":"10.1016/j.tins.2024.05.003","url":null,"abstract":"<p><p>Members of both the Piezo and transmembrane channel-like (TMC) families are bona fide mammalian mechanotransducers. In a recent study, Zhang, Shao et al. discovered that TMC7, a non-mechanosensitive TMC, inhibits Piezo2-dependent mechanosensation, with implications for the importance of cellular context for Piezo2 channels in normal and pathological responses to mechanical pain.</p>","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":" ","pages":"478-479"},"PeriodicalIF":14.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140959629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in NeurosciencesPub Date : 2024-07-01Epub Date: 2024-05-28DOI: 10.1016/j.tins.2024.04.008
Divyansh Mittal, Rishikesh Narayanan
{"title":"Network motifs in cellular neurophysiology.","authors":"Divyansh Mittal, Rishikesh Narayanan","doi":"10.1016/j.tins.2024.04.008","DOIUrl":"10.1016/j.tins.2024.04.008","url":null,"abstract":"<p><p>Concepts from network science and graph theory, including the framework of network motifs, have been frequently applied in studying neuronal networks and other biological complex systems. Network-based approaches can also be used to study the functions of individual neurons, where cellular elements such as ion channels and membrane voltage are conceptualized as nodes within a network, and their interactions are denoted by edges. Network motifs in this context provide functional building blocks that help to illuminate the principles of cellular neurophysiology. In this review we build a case that network motifs operating within neurons provide tools for defining the functional architecture of single-neuron physiology and neuronal adaptations. We highlight the presence of such computational motifs in the cellular mechanisms underlying action potential generation, neuronal oscillations, dendritic integration, and neuronal plasticity. Future work applying the network motifs perspective may help to decipher the functional complexities of neurons and their adaptation during health and disease.</p>","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":" ","pages":"506-521"},"PeriodicalIF":14.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in NeurosciencesPub Date : 2024-07-01Epub Date: 2024-05-31DOI: 10.1016/j.tins.2024.05.007
Andrea I Luppi, Fernando E Rosas, Pedro A M Mediano, Athena Demertzi, David K Menon, Emmanuel A Stamatakis
{"title":"Unravelling consciousness and brain function through the lens of time, space, and information.","authors":"Andrea I Luppi, Fernando E Rosas, Pedro A M Mediano, Athena Demertzi, David K Menon, Emmanuel A Stamatakis","doi":"10.1016/j.tins.2024.05.007","DOIUrl":"10.1016/j.tins.2024.05.007","url":null,"abstract":"<p><p>Disentangling how cognitive functions emerge from the interplay of brain dynamics and network architecture is among the major challenges that neuroscientists face. Pharmacological and pathological perturbations of consciousness provide a lens to investigate these complex challenges. Here, we review how recent advances about consciousness and the brain's functional organisation have been driven by a common denominator: decomposing brain function into fundamental constituents of time, space, and information. Whereas unconsciousness increases structure-function coupling across scales, psychedelics may decouple brain function from structure. Convergent effects also emerge: anaesthetics, psychedelics, and disorders of consciousness can exhibit similar reconfigurations of the brain's unimodal-transmodal functional axis. Decomposition approaches reveal the potential to translate discoveries across species, with computational modelling providing a path towards mechanistic integration.</p>","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":" ","pages":"551-568"},"PeriodicalIF":14.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141187062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in NeurosciencesPub Date : 2024-07-01Epub Date: 2024-05-22DOI: 10.1016/j.tins.2024.04.007
Calvin J Kersbergen, Dwight E Bergles
{"title":"Priming central sound processing circuits through induction of spontaneous activity in the cochlea before hearing onset.","authors":"Calvin J Kersbergen, Dwight E Bergles","doi":"10.1016/j.tins.2024.04.007","DOIUrl":"10.1016/j.tins.2024.04.007","url":null,"abstract":"<p><p>Sensory systems experience a period of intrinsically generated neural activity before maturation is complete and sensory transduction occurs. Here we review evidence describing the mechanisms and functions of this 'spontaneous' activity in the auditory system. Both ex vivo and in vivo studies indicate that this correlated activity is initiated by non-sensory supporting cells within the developing cochlea, which induce depolarization and burst firing of groups of nearby hair cells in the sensory epithelium, activity that is conveyed to auditory neurons that will later process similar sound features. This stereotyped neural burst firing promotes cellular maturation, synaptic refinement, acoustic sensitivity, and establishment of sound-responsive domains in the brain. While sensitive to perturbation, the developing auditory system exhibits remarkable homeostatic mechanisms to preserve periodic burst firing in deaf mice. Preservation of this early spontaneous activity in the context of deafness may enhance the efficacy of later interventions to restore hearing.</p>","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":" ","pages":"522-537"},"PeriodicalIF":14.6,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11236524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141088867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Subscription and Copyright Information","authors":"","doi":"10.1016/s0166-2236(24)00097-3","DOIUrl":"https://doi.org/10.1016/s0166-2236(24)00097-3","url":null,"abstract":"No Abstract","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":"271 1","pages":""},"PeriodicalIF":15.9,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141523123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Advisory Board and Contents","authors":"","doi":"10.1016/s0166-2236(24)00094-8","DOIUrl":"https://doi.org/10.1016/s0166-2236(24)00094-8","url":null,"abstract":"No Abstract","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":"317 1","pages":""},"PeriodicalIF":15.9,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141523122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in NeurosciencesPub Date : 2024-06-01Epub Date: 2024-05-09DOI: 10.1016/j.tins.2024.04.003
Wenyan Zhang, Hong-Shuo Sun, Xiaoying Wang, Aaron S Dumont, Qiang Liu
{"title":"Cellular senescence, DNA damage, and neuroinflammation in the aging brain.","authors":"Wenyan Zhang, Hong-Shuo Sun, Xiaoying Wang, Aaron S Dumont, Qiang Liu","doi":"10.1016/j.tins.2024.04.003","DOIUrl":"10.1016/j.tins.2024.04.003","url":null,"abstract":"<p><p>Aging may lead to low-level chronic inflammation that increases the susceptibility to age-related conditions, including memory impairment and progressive loss of brain volume. As brain health is essential to promoting healthspan and lifespan, it is vital to understand age-related changes in the immune system and central nervous system (CNS) that drive normal brain aging. However, the relative importance, mechanistic interrelationships, and hierarchical order of such changes and their impact on normal brain aging remain to be clarified. Here, we synthesize accumulating evidence that age-related DNA damage and cellular senescence in the immune system and CNS contribute to the escalation of neuroinflammation and cognitive decline during normal brain aging. Targeting cellular senescence and immune modulation may provide a logical rationale for developing new treatment options to restore immune homeostasis and counteract age-related brain dysfunction and diseases.</p>","PeriodicalId":23325,"journal":{"name":"Trends in Neurosciences","volume":" ","pages":"461-474"},"PeriodicalIF":15.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140904303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}