Journal of Neuroscience Research最新文献_第5页

A strike to the head: Parallels between the pediatric and adult human and the rodent in traumatic brain injury 头部受到撞击小儿、成人和啮齿动物在脑外伤中的相似之处。

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2024-07-02 DOI: 10.1002/jnr.25364

Allie M. Smith, Bernadette E. Grayson

{"title":"A strike to the head: Parallels between the pediatric and adult human and the rodent in traumatic brain injury","authors":"Allie M. Smith, Bernadette E. Grayson","doi":"10.1002/jnr.25364","DOIUrl":"10.1002/jnr.25364","url":null,"abstract":"Traumatic brain injury (TBI) is a condition that occurs commonly in children from infancy through adolescence and is a global health concern. Pediatric TBI presents with a bimodal age distribution, with very young children (0–4 years) and adolescents (15–19 years) more commonly injured. Because children's brains are still developing, there is increased vulnerability to the effects of head trauma, which results in entirely different patterns of injury than in adults. Pediatric TBI has a profound and lasting impact on a child's development and quality of life, resulting in long-lasting consequences to physical, cognitive, and emotional development. Chronic issues like learning disabilities, behavioral problems, and emotional disturbances can develop. Early intervention and ongoing support are critical for minimizing these long-term deficits. Many animal models of TBI exist, and each varies significantly, displaying different characteristics of clinical TBI. The neurodevelopment differs in the rodent from the human in timing and effect, so TBI outcomes in the juvenile rodent can thus vary from the human child. The current review compares findings from preclinical TBI work in juvenile and adult rodents to clinical TBI research in pediatric and adult humans. We focus on the four brain regions most affected by TBI: the prefrontal cortex, corpus callosum, hippocampus, and hypothalamus. Each has its unique developmental projections and thus is impacted by TBI differently. This review aims to compare the healthy neurodevelopment of these four brain regions in humans to the developmental processes in rodents.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 7","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492263","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}

引用次数: 0

Gray matter alterations in Huntington's disease: A meta-analysis of VBM neuroimaging studies 亨廷顿氏病的灰质改变：VBM神经影像学研究的荟萃分析。

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2024-07-02 DOI: 10.1002/jnr.25366

Xi Wang, Yuming Li, Boyi Li, Huifang Shang, Jing Yang

{"title":"Gray matter alterations in Huntington's disease: A meta-analysis of VBM neuroimaging studies","authors":"Xi Wang, Yuming Li, Boyi Li, Huifang Shang, Jing Yang","doi":"10.1002/jnr.25366","DOIUrl":"10.1002/jnr.25366","url":null,"abstract":"Increasing neuroimaging studies have attempted to identify biomarkers of Huntington's disease (HD) progression. Here, we conducted voxel-based meta-analyses of voxel-based morphometry (VBM) studies on HD to investigate the evolution of gray matter volume (GMV) alterations and explore the effects of genetic and clinical features on GMV changes. A systematic review was performed to identify the relevant studies. Meta-analyses of whole-brain VBM studies were performed to assess the regional GMV changes in all HD mutation carriers, in presymptomatic HD (pre-HD), and in symptomatic HD (sym-HD). A quantitative comparison was performed between pre-HD and sym-HD. Meta-regression analyses were used to explore the effects of genetic and clinical features on GMV changes. Twenty-eight studies were included, comparing a total of 1811 HD mutation carriers [including 1150 pre-HD and 560 sym-HD] and 969 healthy controls (HCs). Pre-HD showed decreased GMV in the bilateral caudate nuclei, putamen, insula, anterior cingulate/paracingulate gyri, middle temporal gyri, and left dorsolateral superior frontal gyrus compared with HCs. Compared with pre-HD, GMV decrease in sym-HD extended to the bilateral median cingulate/paracingulate gyri, Rolandic operculum and middle occipital gyri, left amygdala, and superior temporal gyrus. Meta-regression analyses found that age, mean lengths of CAG repeats, and disease burden were negatively associated with GMV atrophy of the bilateral caudate and right insula in all HD mutation carriers. This meta-analysis revealed the pattern of GMV changes from pre-HD to sym-HD, prompting the understanding of HD progression. The pattern of GMV changes may be biomarkers for disease progression in HD.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 7","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492298","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}

引用次数: 0

Newborn auditory brainstem response and sudden infant death syndrome 新生儿听觉脑干反应与婴儿猝死综合症

IF 4.2 3区医学

Journal of Neuroscience Research Pub Date : 2024-06-19 DOI: 10.1002/jnr.25362

Sarah E. Maylott, Guangyu Zeng, Tiffany S. Leung, Catalina Sanchez Montenegro, Alexia Barrios, Arushi Malik, Rafael E. Delgado, Christine F. Delgado, Elizabeth A. Simpson

{"title":"Newborn auditory brainstem response and sudden infant death syndrome","authors":"Sarah E. Maylott, Guangyu Zeng, Tiffany S. Leung, Catalina Sanchez Montenegro, Alexia Barrios, Arushi Malik, Rafael E. Delgado, Christine F. Delgado, Elizabeth A. Simpson","doi":"10.1002/jnr.25362","DOIUrl":"10.1002/jnr.25362","url":null,"abstract":"Sudden infant death syndrome (SIDS)—the sudden and unexplained death of a seemingly healthy infant, <1 year old—may be associated with abnormalities in the brain regions that underlie breathing and arousal during sleep. While post-mortem studies suggest abnormalities in SIDS infants' brainstems, there are no studies of these infants' brainstem function before death. One way to assess the function of the brainstem is with auditory brainstem response (ABR), a routine hearing-screening method that noninvasively measures the brainstem's response to sound. We hypothesize that anomalies in newborns' ABR measures may predict SIDS. Indeed, previous studies identified abnormalities in ABR characteristics in small samples of near-miss SIDS infants hospitalized for infant apnea syndrome. However, there is a need to examine the ABRs of infants who died of SIDS. Therefore, in the current study, we propose integrating two secondary datasets to examine newborns' ABRs (N = 156,972), including those who later died of SIDS (n = ~42; .27 out of every 1000 infants), using existing archived records of neonatal ABR results from a sample of newborns born in Florida. We hypothesize that infants who die from SIDS are more likely than non-SIDS infants to have abnormal ABRs as newborns. Understanding the association between SIDS and ABR may facilitate more accurate identification of an infant's risk for SIDS at birth, enabling increased monitoring, which may facilitate interventions and improve survivorship.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25362","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141419574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Temporal summation of second pain is affected by cognitive load 第二次疼痛的时间总和受认知负荷的影响。

IF 4.2 3区医学

Journal of Neuroscience Research Pub Date : 2024-06-19 DOI: 10.1002/jnr.25363

Lara Rubal-Otero, Antonio Gil-Ugidos, Alberto Jacobo González Villar, María Teresa Carrillo-de-la-Peña

{"title":"Temporal summation of second pain is affected by cognitive load","authors":"Lara Rubal-Otero, Antonio Gil-Ugidos, Alberto Jacobo González Villar, María Teresa Carrillo-de-la-Peña","doi":"10.1002/jnr.25363","DOIUrl":"10.1002/jnr.25363","url":null,"abstract":"This work attempted to clarify the interaction of cognition and pain sensitization during a paradigm of Temporal Summation of Second Pain (TSSP). We analyzed pain ratings and electroencephalographic (EEG) activity obtained from 21 healthy participants during the presentation of four experimental conditions that differed in the manipulation of attention to painful stimuli or working memory load (Attention to hand & TSSP; 0-back & TSSP (low cognitive load); 2-back & TSSP (high cognitive load); 2-back (without pain)). We found that the TSSP was reduced when the attention was diverted and the cognitive load increased, and this reduction was accompanied by higher midfrontal theta activity and lower posterior alpha and central beta activity. Although it is well established that TSSP is a phenomenon that occurs at the spinal level, here we show that it is also affected by supraspinal attentional mechanisms. Delivery of painful repeated stimuli did not affect the performance of the 2-back task but was associated with smaller amplitudes of attentional event-related potentials (ERPs) after standard stimuli (not the target). The study of brain activity during TSSP allowed to clarify the role of top-down attentional modulation in pain sensitization processes. Results contribute to a better understanding of cognitive dysfunction in pain conditions and reinforce the use of therapeutic strategies based on distracting attention away from pain.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25363","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141419575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Progresses in the establishment, evaluation, and application of in vitro blood–brain barrier models 体外血脑屏障模型的建立、评估和应用进展。

IF 4.2 3区医学

Journal of Neuroscience Research Pub Date : 2024-06-10 DOI: 10.1002/jnr.25359

Panfeng Yin, Xianchun Wang

引用次数: 0

Effects of a novel regimen of repetitive transcranial magnetic stimulation (rTMS) on neural remodeling and motor function in adult male mice with ischemic stroke 重复经颅磁刺激（rTMS）对缺血性中风成年雄性小鼠神经重塑和运动功能的影响。

IF 4.2 3区医学

Journal of Neuroscience Research Pub Date : 2024-06-10 DOI: 10.1002/jnr.25358

Wang Peipei, Deng Yu, Lin Xiaoyan, Liu Yunxia, Liang Liuming, Cheng Tongbin, Lv Shaoping

{"title":"Effects of a novel regimen of repetitive transcranial magnetic stimulation (rTMS) on neural remodeling and motor function in adult male mice with ischemic stroke","authors":"Wang Peipei, Deng Yu, Lin Xiaoyan, Liu Yunxia, Liang Liuming, Cheng Tongbin, Lv Shaoping","doi":"10.1002/jnr.25358","DOIUrl":"10.1002/jnr.25358","url":null,"abstract":"Neuroinflammation caused by excessive microglial activation plays a key role in the pathogenesis of ischemic stroke. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuromodulatory technique that has recently been reported to regulate microglial functions and exert anti-inflammatory effects. The intermittent burst stimulation (iTBS) regimen in rTMS improves neuronal excitability. However, whether iTBS exerts its anti-inflammatory effects by stimulating neurons and thereby modulating microglial polarization remains unclear. Motor function was assessed after 1 week of rTMS (iTBS regimen) treatment in adult male mice with occlusion/reperfusion of the middle cerebral artery (MCAO/r) injury. We also investigated the molecular biological alterations associated with microglial polarization using a cell proliferation assay, multiplex cytokine bioassays, and immunofluorescence staining. iTBS regimen can improve balance and motor coordination function, increase spontaneous movement, and improve walking function in mice with early cerebral ischemia injury. Expression levels of IL-1β, TNF-α, and IL-10 increased significantly in mice with MCAO injury. Especially, rTMS significantly increased the number of proliferating cells in the infarcted cortex. The fluorescence intensity of MAP2 in the peri-infarct area of MCAO injured mice was low, but the signal was broader. Compared with MCAO group, the fluorescence intensity of MAP2 in rTMS group was significantly increased. rTMS inhibited pro-inflammatory M1 activation (Iba1+/CD86+) and improved anti-inflammatory M2 activation (Iba1+/CD206+) in the peri-infarct zone, thus significantly changing the phenotypic ratio M1/M2. rTMS improves motor dysfunction and neuroinflammation after cerebral I/R injury in mice by regulating microglial polarization.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300851","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}

引用次数: 0

Early-life and chronic exposure to high-fat diet alters noradrenergic and glutamatergic neurotransmission in the male rat amygdala and hippocampus under cognitive challenges 在认知挑战下，雄性大鼠杏仁核和海马的去甲肾上腺素能和谷氨酸能神经传递会发生改变。

IF 4.2 3区医学

Journal of Neuroscience Research Pub Date : 2024-06-07 DOI: 10.1002/jnr.25360

Daniel Osorio-Gómez, Claudia I. Perez, Pamela Salcedo-Tello, Arturo Hernández-Matias, Susana Hernández-Ramírez, Benjamin Arroyo, Gustavo Pacheco-López, Ranier Gutierrez, Federico Bermúdez-Rattoni, Kioko Guzmán-Ramos, OBETEEN Consortium

{"title":"Early-life and chronic exposure to high-fat diet alters noradrenergic and glutamatergic neurotransmission in the male rat amygdala and hippocampus under cognitive challenges","authors":"Daniel Osorio-Gómez, Claudia I. Perez, Pamela Salcedo-Tello, Arturo Hernández-Matias, Susana Hernández-Ramírez, Benjamin Arroyo, Gustavo Pacheco-López, Ranier Gutierrez, Federico Bermúdez-Rattoni, Kioko Guzmán-Ramos, OBETEEN Consortium","doi":"10.1002/jnr.25360","DOIUrl":"10.1002/jnr.25360","url":null,"abstract":"Childhood obesity increases the risk of health and cognitive disorders in adulthood. Consuming high-fat diets (HFD) during critical neurodevelopmental periods, like childhood, impairs cognition and memory in humans and animals, affecting the function and connectivity of brain structures related to emotional memory. However, the underlying mechanisms of such phenomena need to be better understood. This study aimed to investigate the neurochemical profile of the amygdala and hippocampus, brain structures involved in emotional memory, during the acquisition of conditioned odor aversion in male rats that consumed a HFD from weaning to adulthood. The rats gained weight, experienced metabolic changes, and reduced insulin sensitivity and glucose tolerance. Rats showed enhanced odor aversion memory, contrary to the expected cognitive impairments. This memory enhancement was accompanied by increased noradrenergic and glutamatergic neurotransmission in the amygdala and hippocampus. Importantly, this upregulation was specific to stimuli exposure, as basal neurotransmitter levels remained unaltered by the HFD. Our results suggest that HFD modifies cognitive function by altering neurochemical signaling, in this case, upregulating neurotransmitter levels rendering a stronger memory trace, demonstrating that metabolic dysfunctions do not only trigger exclusively detrimental plasticity processes but also render enhanced plastic effects depending on the type of information.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25360","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

GABAergic system and chloride cotransporters as potential therapeutic targets to mitigate cell death in ischemia GABA 能系统和氯化物共转运体是减轻缺血时细胞死亡的潜在治疗靶点。

IF 4.2 3区医学

Journal of Neuroscience Research Pub Date : 2024-05-29 DOI: 10.1002/jnr.25355

A. A. Nascimento, D. Pereira-Figueiredo, V. P. Borges-Martins, R. C. Kubrusly, K. C. Calaza

{"title":"GABAergic system and chloride cotransporters as potential therapeutic targets to mitigate cell death in ischemia","authors":"A. A. Nascimento, D. Pereira-Figueiredo, V. P. Borges-Martins, R. C. Kubrusly, K. C. Calaza","doi":"10.1002/jnr.25355","DOIUrl":"10.1002/jnr.25355","url":null,"abstract":"Gamma aminobutyric acid (GABA) is a critical inhibitory neurotransmitter in the central nervous system that plays a vital role in modulating neuronal excitability. Dysregulation of GABAergic signaling, particularly involving the cotransporters NKCC1 and KCC2, has been implicated in various pathologies, including epilepsy, schizophrenia, autism spectrum disorder, Down syndrome, and ischemia. NKCC1 facilitates chloride influx, whereas KCC2 mediates chloride efflux via potassium gradient. Altered expression and function of these cotransporters have been associated with excitotoxicity, inflammation, and cellular death in ischemic events characterized by reduced cerebral blood flow, leading to compromised tissue metabolism and subsequent cell death. NKCC1 inhibition has emerged as a potential therapeutic approach to attenuate intracellular chloride accumulation and mitigate neuronal damage during ischemic events. Similarly, targeting KCC2, which regulates chloride efflux, holds promise for improving outcomes and reducing neuronal damage under ischemic conditions. This review emphasizes the critical roles of GABA, NKCC1, and KCC2 in ischemic pathologies and their potential as therapeutic targets. Inhibiting or modulating the activity of these cotransporters represents a promising strategy for reducing neuronal damage, preventing excitotoxicity, and improving neurological outcomes following ischemic events. Furthermore, exploring the interactions between natural compounds and NKCC1/KCC2 provides additional avenues for potential therapeutic interventions for ischemic injury.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161219","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}

引用次数: 0

The influence of accelerated brain aging on coactivation pattern dynamics in Parkinson's disease 大脑加速衰老对帕金森病共激活模式动态的影响。

IF 4.2 3区医学

Journal of Neuroscience Research Pub Date : 2024-05-27 DOI: 10.1002/jnr.25357

Su Yan, Jun Lu, Hongquan Zhu, Tian Tian, Yuanyuan Qin, Yuanhao Li, Wenzhen Zhu

{"title":"The influence of accelerated brain aging on coactivation pattern dynamics in Parkinson's disease","authors":"Su Yan, Jun Lu, Hongquan Zhu, Tian Tian, Yuanyuan Qin, Yuanhao Li, Wenzhen Zhu","doi":"10.1002/jnr.25357","DOIUrl":"10.1002/jnr.25357","url":null,"abstract":"Aging is widely acknowledged as the primary risk factor for brain degeneration, with Parkinson's disease (PD) tending to follow accelerated aging trajectories. We aim to investigate the impact of structural brain aging on the temporal dynamics of a large-scale functional network in PD. We enrolled 62 PD patients and 32 healthy controls (HCs). The level of brain aging was determined by calculating global and local brain age gap estimates (G-brainAGE and L-brainAGE) from structural images. The neural network activity of the whole brain was captured by identifying coactivation patterns (CAPs) from resting-state functional images. Intergroup differences were assessed using the general linear model. Subsequently, a spatial correlation analysis between the L-brainAGE difference map and CAPs was conducted to uncover the anatomical underpinnings of functional alterations. Compared to HCs (−3.73 years), G-brainAGE was significantly higher in PD patients (+1.93 years), who also exhibited widespread elevation in L-brainAGE. G-brainAGE was correlated with disease severity and duration. PD patients spent less time in CAPs involving activated default mode and the fronto-parietal network (DMN-FPN), as well as the sensorimotor and salience network (SMN-SN), and had a reduced transition frequency from other CAPs to the DMN-FPN and SMN-SN CAPs. Furthermore, the pattern of localized brain age acceleration showed spatial similarities with the SMN-SN CAP. Accelerated structural brain aging in PD adversely affects brain function, manifesting as dysregulated brain network dynamics. These findings provide insights into the neuropathological mechanisms underlying neurodegenerative diseases and imply the possibility of interventions for modifying PD progression by slowing the brain aging process.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141158495","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}

引用次数: 0

The interplay between glucose and ketone bodies in neural stem cell metabolism 葡萄糖和酮体在神经干细胞新陈代谢中的相互作用。

IF 4.2 3区医学

Journal of Neuroscience Research Pub Date : 2024-05-21 DOI: 10.1002/jnr.25342

Joseph W. Molloy, Denis Barry

{"title":"The interplay between glucose and ketone bodies in neural stem cell metabolism","authors":"Joseph W. Molloy, Denis Barry","doi":"10.1002/jnr.25342","DOIUrl":"10.1002/jnr.25342","url":null,"abstract":"Glucose is the primary energy source for neural stem cells (NSCs), supporting their proliferation, differentiation, and quiescence. However, the high demand for glucose during brain development often exceeds its supply, leading to the utilization of alternative energy sources including ketone bodies. Ketone bodies, including β-hydroxybutyrate, are short-chain fatty acids produced through hepatic ketogenesis and play a crucial role in providing energy and the biosynthetic components for NSCs when required. The interplay between glucose and ketone metabolism influences NSC behavior and fate decisions, and disruptions in these metabolic pathways have been linked to neurodevelopmental, neuropsychiatric, and neurodegenerative disorders. Additionally, ketone bodies exert neuroprotective effects on NSCs and modulate cellular responses to oxidative stress, energy maintenance, deacetylation, and inflammation. As such, understanding the interdependence of glucose and ketone metabolism in NSCs is crucial to understanding their roles in NSC function and their implications for neurological conditions. This article reviews the mechanisms of glucose and ketone utilization in NSCs, their impact on NSC function, and the therapeutic potential of targeting these metabolic pathways in neurological disorders.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25342","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141076021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0