{"title":"From the Eyes to the Suffering Brain: Can Eye Tracking be Considered as a Significant Digital Biomarker for Neurological Diseases?","authors":"Sonja Cecchetti, Upal Roy, Marco Cavallo","doi":"10.31083/j.jin2309167","DOIUrl":"https://doi.org/10.31083/j.jin2309167","url":null,"abstract":"","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 9","pages":"167"},"PeriodicalIF":2.5,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vaia Gialama, Vasileios Siokas, Ioannis Liampas, Zisis Tsouris, Polyxeni Stamati, Paraskevi Aslanidou, Antonios Provatas, Vana Tsimourtou, Georgia Xiromerisiou, Dimitrios P Bogdanos, Efthimios Dardiotis
Alzheimer's Disease (AD) is a progressive neurodegenerative disease and the main cause of dementia. Its etiology remains largely unclear, though genetic and environmental factors appear to confer susceptibility to AD development. This study assessed the role of ATP-binding Cassette A Subfamily 7 (ABCA7) genetic polymorphisms, as ongoing research suggests they have a role in the development of AD. We conducted a PubMed, Google Scholar, and Scopus search to identify and assess all AD studies examining ABCA7 variants in different populations and ethnicities. The last search was conducted on February 8, 2023. Inclusion and exclusion criteria were applied and only the studies that met the inclusion criteria were included in this review. Seventeen studies were finally included. According to the results, ABCA7 variants infer different risks for AD among populations with different ancestries. African American populations show a higher risk for AD, carrying the five novel variants rs115550680, rs142076058, rs10405305, rs3764647, and rs567222111. Asian populations also have an increased risk for AD, harboring three variants. ABCA7 genetic variability contributes to AD development and shows racial disparities. African American and Asian populations seem to be at greater risk of developing AD. These results may assist future research efforts for the early and accurate diagnosis of AD. Moreover, further exploration of the mechanisms of ABCA7 in the context of AD could identify potential therapeutic targets.
{"title":"Alzheimer's Disease and Effects of <i>ABCA7</i> Polymorphisms: A Review.","authors":"Vaia Gialama, Vasileios Siokas, Ioannis Liampas, Zisis Tsouris, Polyxeni Stamati, Paraskevi Aslanidou, Antonios Provatas, Vana Tsimourtou, Georgia Xiromerisiou, Dimitrios P Bogdanos, Efthimios Dardiotis","doi":"10.31083/j.jin2309164","DOIUrl":"10.31083/j.jin2309164","url":null,"abstract":"<p><p>Alzheimer's Disease (AD) is a progressive neurodegenerative disease and the main cause of dementia. Its etiology remains largely unclear, though genetic and environmental factors appear to confer susceptibility to AD development. This study assessed the role of ATP-binding Cassette A Subfamily 7 (<i>ABCA7</i>) genetic polymorphisms, as ongoing research suggests they have a role in the development of AD. We conducted a PubMed, Google Scholar, and Scopus search to identify and assess all AD studies examining <i>ABCA7</i> variants in different populations and ethnicities. The last search was conducted on February 8, 2023. Inclusion and exclusion criteria were applied and only the studies that met the inclusion criteria were included in this review. Seventeen studies were finally included. According to the results, <i>ABCA7</i> variants infer different risks for AD among populations with different ancestries. African American populations show a higher risk for AD, carrying the five novel variants <i>rs115550680</i>, <i>rs142076058</i>, <i>rs10405305</i>, <i>rs3764647</i>, and <i>rs567222111</i>. Asian populations also have an increased risk for AD, harboring three variants. <i>ABCA7</i> genetic variability contributes to AD development and shows racial disparities. African American and Asian populations seem to be at greater risk of developing AD. These results may assist future research efforts for the early and accurate diagnosis of AD. Moreover, further exploration of the mechanisms of ABCA7 in the context of AD could identify potential therapeutic targets.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 9","pages":"164"},"PeriodicalIF":2.5,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Epidemiological studies show that individuals with obesity are more likely to develop Alzheimer's disease (AD) than those who do not have obesity. However, the mechanisms underlying the relationship between obesity and AD are not entirely unclear. Here, we have reviewed and analyzed relevant articles published in the literature and found that obesity has correlation or potential increase in the levels of β-amyloid (Aβ) protein, which may explain why people with obesity are more likely to suffer from AD. Additionally, the published findings point to the roles of obesity-related metabolic disorders, such as diabetes, inflammation, oxidative stress, and imbalance in gut microbiota in Aβ accumulation caused by obesity. Therefore, in-depth experimental and clinical studies on these mechanisms in the future may help shed light on appropriate prevention and treatment strategies for AD, such as dietary changes and regular exercise to reverse or prevent obesity and related metabolic disorders.
{"title":"Mechanisms Underlying Obesity-induced Aβ Accumulation in Alzheimer's Disease: A Qualitative Review.","authors":"Wei Wen, Shu-Ming Huang, Bo Zhang","doi":"10.31083/j.jin2309163","DOIUrl":"10.31083/j.jin2309163","url":null,"abstract":"<p><p>Epidemiological studies show that individuals with obesity are more likely to develop Alzheimer's disease (AD) than those who do not have obesity. However, the mechanisms underlying the relationship between obesity and AD are not entirely unclear. Here, we have reviewed and analyzed relevant articles published in the literature and found that obesity has correlation or potential increase in the levels of β-amyloid (Aβ) protein, which may explain why people with obesity are more likely to suffer from AD. Additionally, the published findings point to the roles of obesity-related metabolic disorders, such as diabetes, inflammation, oxidative stress, and imbalance in gut microbiota in Aβ accumulation caused by obesity. Therefore, in-depth experimental and clinical studies on these mechanisms in the future may help shed light on appropriate prevention and treatment strategies for AD, such as dietary changes and regular exercise to reverse or prevent obesity and related metabolic disorders.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 9","pages":"163"},"PeriodicalIF":2.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jiliang Kang, Junyue Lu, Shuang Gong, Yan Yu, Mengbi Gu, Siyang Wu, Min Tang, Youliang Wen
Background: The aim of this preliminary study was to investigate the similarities and differences in cortical activation patterns during the swallowing of water, acetic acid solution and salt solution in healthy adults using functional near-infrared spectroscopy (fNIRS).
Methods: Eighteen right-handed healthy adults were recruited and fNIRS was used to measure changes in concentrations of oxygenated hemoglobin (HbO2) and deoxygenated hemoglobin (HbR) in 35 channels during the swallowing of water, acetic acid solution and salt solution. The task-based experiment used a block-design in which participants alternated between resting blocks of 30 s and task blocks (swallowing water, acetic acid solution, or salt solution) of 30 s, repeated six times. Participants remained still during the resting blocks and performed a swallowing action every 6 s during the task blocks. Data preprocessing was conducted using NirSpark software and statistical analyses were performed using either one-sample or paired t-tests to compare differences in cortical activation in healthy participants between swallowing a water and acetic acid solution, as well as swallowing a water and salt solution.
Results: Compared to the resting state, nine brain regions, including primary somatosensory cortex (S1), primary motor cortex (M1), dorsolateral prefrontal cortex (DLPFC), Wernicke's area, premotor cortex (PMC), supplementary motor area (SMA), inferior frontal cortex (IFC), orbitofrontal cortex (OFC) and frontopolar area, were commonly activated during the process of swallowing water, acetic acid solution, and salt solution. The DLPFC, Broca's area, PMC and SMA showed higher activation levels during the swallowing of acetic acid solution when compared to swallowing water, with statistically significant differences (p < 0.05). The frontopolar area and OFC exhibited higher activation during the swallowing of salt solution when compared to water, also with statistically significant differences (p < 0.05).
Conclusions: Multiple brain regions were activated during the swallowing of water, acetic acid solution and salt solution in healthy adults. Moreover, swallowing acetic acid solution leads to stronger activation of DLPFC, Broca's area, PMC and SMA, while swallowing salt solution leads to stronger activation of the frontopolar area and OFC.
{"title":"Change of Cerebral Hemodynamic Signals during the Process of Swallowing Water, Acetic Acid Solution and Salt Solution in Healthy Adults: An fNIRS Study.","authors":"Jiliang Kang, Junyue Lu, Shuang Gong, Yan Yu, Mengbi Gu, Siyang Wu, Min Tang, Youliang Wen","doi":"10.31083/j.jin2309162","DOIUrl":"https://doi.org/10.31083/j.jin2309162","url":null,"abstract":"<p><strong>Background: </strong>The aim of this preliminary study was to investigate the similarities and differences in cortical activation patterns during the swallowing of water, acetic acid solution and salt solution in healthy adults using functional near-infrared spectroscopy (fNIRS).</p><p><strong>Methods: </strong>Eighteen right-handed healthy adults were recruited and fNIRS was used to measure changes in concentrations of oxygenated hemoglobin (HbO<sub>2</sub>) and deoxygenated hemoglobin (HbR) in 35 channels during the swallowing of water, acetic acid solution and salt solution. The task-based experiment used a block-design in which participants alternated between resting blocks of 30 s and task blocks (swallowing water, acetic acid solution, or salt solution) of 30 s, repeated six times. Participants remained still during the resting blocks and performed a swallowing action every 6 s during the task blocks. Data preprocessing was conducted using NirSpark software and statistical analyses were performed using either one-sample or paired <i>t</i>-tests to compare differences in cortical activation in healthy participants between swallowing a water and acetic acid solution, as well as swallowing a water and salt solution.</p><p><strong>Results: </strong>Compared to the resting state, nine brain regions, including primary somatosensory cortex (S1), primary motor cortex (M1), dorsolateral prefrontal cortex (DLPFC), Wernicke's area, premotor cortex (PMC), supplementary motor area (SMA), inferior frontal cortex (IFC), orbitofrontal cortex (OFC) and frontopolar area, were commonly activated during the process of swallowing water, acetic acid solution, and salt solution. The DLPFC, Broca's area, PMC and SMA showed higher activation levels during the swallowing of acetic acid solution when compared to swallowing water, with statistically significant differences (<i>p</i> < 0.05). The frontopolar area and OFC exhibited higher activation during the swallowing of salt solution when compared to water, also with statistically significant differences (<i>p</i> < 0.05).</p><p><strong>Conclusions: </strong>Multiple brain regions were activated during the swallowing of water, acetic acid solution and salt solution in healthy adults. Moreover, swallowing acetic acid solution leads to stronger activation of DLPFC, Broca's area, PMC and SMA, while swallowing salt solution leads to stronger activation of the frontopolar area and OFC.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 9","pages":"162"},"PeriodicalIF":2.5,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bingshan Xu, Chunrong Lin, Yiwen Wang, Hong Wang, Yao Liu, Xiaojun Wang
Background: The clinical application of 10 Hz repetitive transcranil magnetic stimulation (rTMS) remains limited despite its demonstrated effectiveness in enhancing cortical excitability and improving cognitive function. The present study used a novel stimulus target [left dorsolateral prefrontal cortex + primary motor cortex] to facilitate the enhancement of cognitive function through the bidirectional promotion of cognitive and motor functions; Methods: Post-stroke cognitive impairment patients (n = 48) were randomly assigned to receive either dual-target, single-target, or sham rTMS for 4 weeks. Before and after 4 weeks of treatment, participants were asked to complete the Montreal Cognitive Assessment (MoCA) test, the Modified Barthel Index (MBI), the Trail-making Test (TMT), and the Digital Span Test (DST). In addition, the levels of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) in serum were also measured.
Results: After adjusting for pre-intervention (baseline) MoCA scores, the post-intervention MoCA scores varied significantly. After post-hoc analysis, differences existed between the post-treatment scores of the dual-target rTMS group and the sham rTMS group (the experimental group scores were significantly higher), and between those of the dual-target rTMS group and the single-target rTMS group (the dual-target rTMS scores were significantly higher). The serum VEGF levels of the dual-target rTMS group were significantly higher those that of the sham rTMS group.
Conclusions: The present study presented data showing that a dual-target rTMS therapy is effective for Post-stroke cognitive impairment (PSCI). The stimulation exhibited remarkable efficacy, suggesting that dual-target stimulation (left dorsolateral prefrontal cortex+motor cortex (L-DLPFC+M1)) holds promise as a potential target for TMS therapy in individuals with cognitive impairment after stroke.
{"title":"Using Dual-Target rTMS, Single-Target rTMS, or Sham rTMS on Post-Stroke Cognitive Impairment.","authors":"Bingshan Xu, Chunrong Lin, Yiwen Wang, Hong Wang, Yao Liu, Xiaojun Wang","doi":"10.31083/j.jin2308161","DOIUrl":"https://doi.org/10.31083/j.jin2308161","url":null,"abstract":"<p><strong>Background: </strong>The clinical application of 10 Hz repetitive transcranil magnetic stimulation (rTMS) remains limited despite its demonstrated effectiveness in enhancing cortical excitability and improving cognitive function. The present study used a novel stimulus target [left dorsolateral prefrontal cortex + primary motor cortex] to facilitate the enhancement of cognitive function through the bidirectional promotion of cognitive and motor functions; Methods: Post-stroke cognitive impairment patients (<i>n</i> = 48) were randomly assigned to receive either dual-target, single-target, or sham rTMS for 4 weeks. Before and after 4 weeks of treatment, participants were asked to complete the Montreal Cognitive Assessment (MoCA) test, the Modified Barthel Index (MBI), the Trail-making Test (TMT), and the Digital Span Test (DST). In addition, the levels of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) in serum were also measured.</p><p><strong>Results: </strong>After adjusting for pre-intervention (baseline) MoCA scores, the post-intervention MoCA scores varied significantly. After post-hoc analysis, differences existed between the post-treatment scores of the dual-target rTMS group and the sham rTMS group (the experimental group scores were significantly higher), and between those of the dual-target rTMS group and the single-target rTMS group (the dual-target rTMS scores were significantly higher). The serum VEGF levels of the dual-target rTMS group were significantly higher those that of the sham rTMS group.</p><p><strong>Conclusions: </strong>The present study presented data showing that a dual-target rTMS therapy is effective for Post-stroke cognitive impairment (PSCI). The stimulation exhibited remarkable efficacy, suggesting that dual-target stimulation (left dorsolateral prefrontal cortex+motor cortex (L-DLPFC+M1)) holds promise as a potential target for TMS therapy in individuals with cognitive impairment after stroke.</p><p><strong>Clinical trial registration: </strong>No: ChiCTR220066184. Registered 26 November, 2022, https://www.chictr.org.cn.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"161"},"PeriodicalIF":2.5,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Li Zhang, Yating Chen, Guilan Huang, Yao Qian, Yu Yao, Lianxin Song, Yi Shao, Nan Jiang, Chengpan Liang, Hewei Wang, Bin Su
Background: Previous studies have found that inhibitory priming with continuous theta burst stimulation (cTBS) can enhance the effect of subsequent excitatory conditioning stimuli with intermittent theta burst stimulation (iTBS) in the upper limbs. However, whether this combined stimulation approach elicits a comparable compensatory response in the lower extremities remains unclear. This study aimed to investigate how cTBS preconditioning modulated the effect of iTBS on motor cortex excitability related to the lower limb in healthy individuals.
Methods: Using a randomised cross-over design, a total of 25 healthy participants (19 females, mean age = 24.80 yr) were recruited to undergo three different TBS protocols (cTBS + iTBS, sham cTBS + iTBS, sham cTBS + sham iTBS) in a random order. Each TBS intervention was administered with one-week intervals. cTBS and iTBS were administered at an intensity of 80% active motor threshold (AMT) delivering a total of 600 pulses. Before intervention (T0), immediately following intervention (T1), and 20 min after intervention (T2), the corticomotor excitability was measured for the tibialis anterior muscle of participants' non-dominant leg using a Magneuro100 stimulator and matched double-cone coil. The average amplitude of the motor-evoked potential (MEP) induced by applying 20 consecutive monopulse stimuli at an intensity of 130% resting motor threshold (RMT) was collected and analysed.
Results: Compare with T0 time, the MEP amplitude (raw and normalised) at T1 and T2 showed a statistically significant increase following the cTBS + iTBS protocol (p < 0.01), but no significant differences were observed in amplitude changes following other protocols (sham cTBS + iTBS and sham cTBS + sham iTBS) (p > 0.05). Furthermore, no statistically significant difference was found among the three protocols at any given time point (p > 0.05).
Conclusions: Preconditioning the lower extremity motor cortex with cTBS prior to iTBS intervention can promptly enhance its excitability in healthy participants. This effect persists for a minimum duration of 20 min.
{"title":"Immediate Effects of Preconditioning Intermittent Theta Burst Stimulation on Lower Extremity Motor Cortex Excitability in Healthy Participants.","authors":"Li Zhang, Yating Chen, Guilan Huang, Yao Qian, Yu Yao, Lianxin Song, Yi Shao, Nan Jiang, Chengpan Liang, Hewei Wang, Bin Su","doi":"10.31083/j.jin2308160","DOIUrl":"https://doi.org/10.31083/j.jin2308160","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have found that inhibitory priming with continuous theta burst stimulation (cTBS) can enhance the effect of subsequent excitatory conditioning stimuli with intermittent theta burst stimulation (iTBS) in the upper limbs. However, whether this combined stimulation approach elicits a comparable compensatory response in the lower extremities remains unclear. This study aimed to investigate how cTBS preconditioning modulated the effect of iTBS on motor cortex excitability related to the lower limb in healthy individuals.</p><p><strong>Methods: </strong>Using a randomised cross-over design, a total of 25 healthy participants (19 females, mean age = 24.80 yr) were recruited to undergo three different TBS protocols (cTBS + iTBS, sham cTBS + iTBS, sham cTBS + sham iTBS) in a random order. Each TBS intervention was administered with one-week intervals. cTBS and iTBS were administered at an intensity of 80% active motor threshold (AMT) delivering a total of 600 pulses. Before intervention (T0), immediately following intervention (T1), and 20 min after intervention (T2), the corticomotor excitability was measured for the tibialis anterior muscle of participants' non-dominant leg using a Magneuro100 stimulator and matched double-cone coil. The average amplitude of the motor-evoked potential (MEP) induced by applying 20 consecutive monopulse stimuli at an intensity of 130% resting motor threshold (RMT) was collected and analysed.</p><p><strong>Results: </strong>Compare with T0 time, the MEP amplitude (raw and normalised) at T1 and T2 showed a statistically significant increase following the cTBS + iTBS protocol (<i>p</i> < 0.01), but no significant differences were observed in amplitude changes following other protocols (sham cTBS + iTBS and sham cTBS + sham iTBS) (<i>p</i> > 0.05). Furthermore, no statistically significant difference was found among the three protocols at any given time point (<i>p</i> > 0.05).</p><p><strong>Conclusions: </strong>Preconditioning the lower extremity motor cortex with cTBS prior to iTBS intervention can promptly enhance its excitability in healthy participants. This effect persists for a minimum duration of 20 min.</p><p><strong>Clinical trial registration: </strong>No: ChiCTR2300069315. Registered 13 March, 2023, https://www.chictr.org.cn.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"160"},"PeriodicalIF":2.5,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><strong>Background: </strong>Peripheral nerve injury is a challenging orthopedic issue in clinical management that often leads to limb dysfunction or even disability in severe cases. A thorough exploration of the repair process of peripheral nerve injury and the underlying mechanism contributes to formulate more effective therapeutic strategies.</p><p><strong>Methods: </strong>In the present study, we established a sciatic nerve transection injury model in Sprague-Dawley (SD) rats. A 12-week compensatory repair of sciatic nerve transection injury using a chitin cannula for small gap anastomosis was then performed via sleeve jointing the proximal common peroneal nerve to the distal tibial nerve and common peroneal nerve, with a 2 mm interval. Compensatory repair via small gap amplification was observed via gross observation of nerve specimen, osmic acid staining, and electrophysiological stimulation of sciatic nerve branches of the tibial and common peroneal nerve. Rat limbs were observed, and the functional recovery of effector muscles of the gastrocnemius and tibialis anterior muscles was assessed through weighing the muscle wet weight, Hematoxylin and Eosin (H&E) staining, and muscle strength detection. H&E staining, Masson staining, and toluidine blue staining were performed to observe the morphological changes of the dorsal root ganglion. Positive expressions of key proteins involved in the Phosphatase and tensin homologue deleted on chromosome ten (PTEN)-protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway, including PTEN, AKT, mTOR, Toll-like receptor 4 (TLR4), and Caspase9 in the dorsal root ganglion during compensatory repair of sciatic nerve after injury via small gap amplification, were detected by immunohistochemical staining.</p><p><strong>Results: </strong>It is found that the compensatory repair of sciatic nerve transection injury using a chitin cannula for small gap anastomosis via sleeve jointing effectively restored the continuity, number of myelinated nerve fibers, and nerve conduction velocity. It promoted toe abduction recovery, improved muscle fiber morphology and increased the wet weight and muscle strength of the gastrocnemius muscle and tibialis anterior muscle. Moreover, it increased the number of neurons and nerve fibers, and improved their morphology. Downregulated PTEN, TLR4, and Caspase9 in the dorsal root ganglia and upregulated AKT and mTOR were observed after small gap amplification than those of the transection injury group, which were closer to those of the control group.</p><p><strong>Conclusions: </strong>Compensatory repair of sciatic nerve transection injury using a chitin cannula for small gap anastomosis via sleeve jointing can restore the morphology and function of the sciatic nerve, effector muscles, and corresponding dorsal root ganglia by activating the PTEN-AKT/mTOR signaling pathway in the dorsal root ganglia. Our findings provide novel therapeutic targets for peripheral ne
{"title":"The Exploratory Study of the PTEN-AKT/mTOR Signaling Pathway in the Corresponding Dorsal Root Ganglion during Compensatory Repair via Small Gap Amplification in Sciatic Nerve Injury.","authors":"Fei Yu, Tiantian Qi, Yusong Yuan, Jian Weng, Tianbing Wang, Yuhui Kou, Hui Zeng","doi":"10.31083/j.jin2308157","DOIUrl":"10.31083/j.jin2308157","url":null,"abstract":"<p><strong>Background: </strong>Peripheral nerve injury is a challenging orthopedic issue in clinical management that often leads to limb dysfunction or even disability in severe cases. A thorough exploration of the repair process of peripheral nerve injury and the underlying mechanism contributes to formulate more effective therapeutic strategies.</p><p><strong>Methods: </strong>In the present study, we established a sciatic nerve transection injury model in Sprague-Dawley (SD) rats. A 12-week compensatory repair of sciatic nerve transection injury using a chitin cannula for small gap anastomosis was then performed via sleeve jointing the proximal common peroneal nerve to the distal tibial nerve and common peroneal nerve, with a 2 mm interval. Compensatory repair via small gap amplification was observed via gross observation of nerve specimen, osmic acid staining, and electrophysiological stimulation of sciatic nerve branches of the tibial and common peroneal nerve. Rat limbs were observed, and the functional recovery of effector muscles of the gastrocnemius and tibialis anterior muscles was assessed through weighing the muscle wet weight, Hematoxylin and Eosin (H&E) staining, and muscle strength detection. H&E staining, Masson staining, and toluidine blue staining were performed to observe the morphological changes of the dorsal root ganglion. Positive expressions of key proteins involved in the Phosphatase and tensin homologue deleted on chromosome ten (PTEN)-protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway, including PTEN, AKT, mTOR, Toll-like receptor 4 (TLR4), and Caspase9 in the dorsal root ganglion during compensatory repair of sciatic nerve after injury via small gap amplification, were detected by immunohistochemical staining.</p><p><strong>Results: </strong>It is found that the compensatory repair of sciatic nerve transection injury using a chitin cannula for small gap anastomosis via sleeve jointing effectively restored the continuity, number of myelinated nerve fibers, and nerve conduction velocity. It promoted toe abduction recovery, improved muscle fiber morphology and increased the wet weight and muscle strength of the gastrocnemius muscle and tibialis anterior muscle. Moreover, it increased the number of neurons and nerve fibers, and improved their morphology. Downregulated PTEN, TLR4, and Caspase9 in the dorsal root ganglia and upregulated AKT and mTOR were observed after small gap amplification than those of the transection injury group, which were closer to those of the control group.</p><p><strong>Conclusions: </strong>Compensatory repair of sciatic nerve transection injury using a chitin cannula for small gap anastomosis via sleeve jointing can restore the morphology and function of the sciatic nerve, effector muscles, and corresponding dorsal root ganglia by activating the PTEN-AKT/mTOR signaling pathway in the dorsal root ganglia. Our findings provide novel therapeutic targets for peripheral ne","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"157"},"PeriodicalIF":2.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Sleep patterns often shift as people age, a phenomenon frequently associated with the onset of neurodegenerative conditions. Additionally, distinct alterations occur in brain structure as individuals grow older, particularly within the hippocampus, a region known for its role in cognition and sleep regulation. Yet, how exactly do changes in sleep relate to specific subfields within the hippocampus is still unclear.
Methods: We conducted a study involving non-demented healthy adults from the Aiginition Longitudinal Biomarker Investigation Of Neurodegeneration (ALBION) cohort. Participants underwent objective sleep measurements using wrist Actiwatch and WatchPAT devices. Further, all participants underwent the same Magnetic Resonance Imaging (MRI) protocol, including a 3D high resolution T1-weighted sequence, on the same 3.0 Tesla MRI scanner using an eight-channel head coil. The study aimed to examine the relationship between objectively measured sleep metrics and the morphology of twenty-two distinct hippocampal subregions.
Results: In total, 75 non-demented participants with 63 mean years of age were included in the study. Results indicated that a higher frequency of awakenings during sleep was associated with increased volume in the right presubiculum body (beta = 0.630, p False Discovery Rate (FDR) <0.036). Longer sleep duration showed a tendency to be associated with smaller volumes of the right presubiculum body, hinting at a possible negative impact of prolonged sleep on this brain region. Similar trends were observed regarding sleep apnea and the presubiculum body volume. Further analysis based on age stratification revealed that in younger participants, longer sleep duration was linked to decreased volume of the presubiculum body, while a greater number of awakenings was correlated with increased volume of the same region. Among older participants, higher frequencies of awakenings were associated with larger volumes in various hippocampal subfields.
Conclusions: These findings shed light on the complex relationship between sleep characteristics and brain structure, highlighting potential age-related differences. The study provides valuable insights into how sleep disruptions may impact hippocampal morphology and cognitive function of cognitively healthy adults. Further research is warranted to elucidate the underlying mechanisms and implications for neurodegenerative diseases.
{"title":"Objective Sleep Function is Associated with Hippocampal Subfield Volumes in Community-Dwelling Adults.","authors":"Niki Mourtzi, Angeliki Tsapanou, Renia Morfakidou, Georgia Angelopoulou, Vasilios Constantinides, Eva Ntanasi, Eirini Mamalaki, Mary Yannakoulia, Efstratios Karavasilis, Foteini Christidi, Georgios Velonakis, Nikolaos Scarmeas","doi":"10.31083/j.jin2308159","DOIUrl":"https://doi.org/10.31083/j.jin2308159","url":null,"abstract":"<p><strong>Background: </strong>Sleep patterns often shift as people age, a phenomenon frequently associated with the onset of neurodegenerative conditions. Additionally, distinct alterations occur in brain structure as individuals grow older, particularly within the hippocampus, a region known for its role in cognition and sleep regulation. Yet, how exactly do changes in sleep relate to specific subfields within the hippocampus is still unclear.</p><p><strong>Methods: </strong>We conducted a study involving non-demented healthy adults from the Aiginition Longitudinal Biomarker Investigation Of Neurodegeneration (ALBION) cohort. Participants underwent objective sleep measurements using wrist Actiwatch and WatchPAT devices. Further, all participants underwent the same Magnetic Resonance Imaging (MRI) protocol, including a 3D high resolution T1-weighted sequence, on the same 3.0 Tesla MRI scanner using an eight-channel head coil. The study aimed to examine the relationship between objectively measured sleep metrics and the morphology of twenty-two distinct hippocampal subregions.</p><p><strong>Results: </strong>In total, 75 non-demented participants with 63 mean years of age were included in the study. Results indicated that a higher frequency of awakenings during sleep was associated with increased volume in the right presubiculum body (beta = 0.630, <i>p</i> False Discovery Rate (FDR) <0.036). Longer sleep duration showed a tendency to be associated with smaller volumes of the right presubiculum body, hinting at a possible negative impact of prolonged sleep on this brain region. Similar trends were observed regarding sleep apnea and the presubiculum body volume. Further analysis based on age stratification revealed that in younger participants, longer sleep duration was linked to decreased volume of the presubiculum body, while a greater number of awakenings was correlated with increased volume of the same region. Among older participants, higher frequencies of awakenings were associated with larger volumes in various hippocampal subfields.</p><p><strong>Conclusions: </strong>These findings shed light on the complex relationship between sleep characteristics and brain structure, highlighting potential age-related differences. The study provides valuable insights into how sleep disruptions may impact hippocampal morphology and cognitive function of cognitively healthy adults. Further research is warranted to elucidate the underlying mechanisms and implications for neurodegenerative diseases.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"159"},"PeriodicalIF":2.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To investigate the relationship of diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) parameters with dysfunction in acute focal cerebral ischemia (ACI) rabbits.
Methods: The model of ACI in the middle cerebral artery was made using 30 adult male New Zealand rabbits. The dysfunction severities of the ACI rabbits were assessed using Purdy's score. A paired-sample rank sum test was adopted to compare the abnormal signal zone (ASZ) volumes from T2 weighted imaging (T2WI), dynamic susceptibility contrast-enhanced (DSC) imaging, and DWI with a relative cerebral blood flow (rCBF) map; correlations were analyzed between the volume of each ASZ and Purdy's score by Spearman's rank correlation coefficient. The degree of necrotic and apoptotic cells was evaluated in the ASZ from DWI and DSC PWI-DWI mismatch (PDM) zone. Correlations were analyzed between the index of cellular damage and Purdy's score, the volume of ASZs by Spearman's rank correlation coefficient.
Results: The ASZ volumes from DSC-PWI and the rCBF maps were larger than those from DWI (p < 0.001 and p < 0.001, respectively); those from the rCBF map (Z = 0.959, p < 0.001) and DSC-PWI (Z = 0.970, p < 0.001) were positively correlated with DWI; a positive correlation was found between Purdy's score and the ASZ volumes from DSC-PWI (Z = 0.889, p < 0.001), DWI (Z = 0.921, p < 0.001), and rCBF (Z = 0.891, p < 0.001). A significant difference was observed between the ASZ from DWI and the PDM zone in terms of the degree of necrotic (p < 0.001) and apoptotic cells (p < 0.001). The degree of cellular damage in the ASZ of DWI and PDM zone had no relationship with Purdy's score and the volumes of ASZs.
Conclusion: The ASZ volumes from DSC-PWI, rCBF, and particularly DWI reflected the level of dysfunction in rabbits with ACI.
{"title":"Diffusion- and Perfusion-Weighted Imaging to Detect Neurological Deficits in Acute Focal Cerebral Ischemia in Rabbits.","authors":"Yu Zhang, Xuefei Deng, Jiangdong Chu, Qian Zhang, Xiangwei Luo, Xingxing Wang","doi":"10.31083/j.jin2308156","DOIUrl":"https://doi.org/10.31083/j.jin2308156","url":null,"abstract":"<p><strong>Purpose: </strong>To investigate the relationship of diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) parameters with dysfunction in acute focal cerebral ischemia (ACI) rabbits.</p><p><strong>Methods: </strong>The model of ACI in the middle cerebral artery was made using 30 adult male New Zealand rabbits. The dysfunction severities of the ACI rabbits were assessed using Purdy's score. A paired-sample rank sum test was adopted to compare the abnormal signal zone (ASZ) volumes from T<sub>2</sub> weighted imaging (T<sub>2</sub>WI), dynamic susceptibility contrast-enhanced (DSC) imaging, and DWI with a relative cerebral blood flow (rCBF) map; correlations were analyzed between the volume of each ASZ and Purdy's score by Spearman's rank correlation coefficient. The degree of necrotic and apoptotic cells was evaluated in the ASZ from DWI and DSC PWI-DWI mismatch (PDM) zone. Correlations were analyzed between the index of cellular damage and Purdy's score, the volume of ASZs by Spearman's rank correlation coefficient.</p><p><strong>Results: </strong>The ASZ volumes from DSC-PWI and the rCBF maps were larger than those from DWI (<i>p</i> < 0.001 and <i>p</i> < 0.001, respectively); those from the rCBF map (Z = 0.959, <i>p</i> < 0.001) and DSC-PWI (Z = 0.970, <i>p</i> < 0.001) were positively correlated with DWI; a positive correlation was found between Purdy's score and the ASZ volumes from DSC-PWI (Z = 0.889, <i>p</i> < 0.001), DWI (Z = 0.921, <i>p</i> < 0.001), and rCBF (Z = 0.891, <i>p</i> < 0.001). A significant difference was observed between the ASZ from DWI and the PDM zone in terms of the degree of necrotic (<i>p</i> < 0.001) and apoptotic cells (<i>p</i> < 0.001). The degree of cellular damage in the ASZ of DWI and PDM zone had no relationship with Purdy's score and the volumes of ASZs.</p><p><strong>Conclusion: </strong>The ASZ volumes from DSC-PWI, rCBF, and particularly DWI reflected the level of dysfunction in rabbits with ACI.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"156"},"PeriodicalIF":2.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Most acute cerebral infarctions (ACI) may develop vascular dementia (VD), which involves almost all types of cognitive impairment. Unfortunately, there is currently no effective treatment for VD. Most patients exhibit mild cognitive impairment (MCI) before the development of VD. N-butyl-phthalide (NBP) is used to treat ACI and improve cognitive function. The oxygen and glucose deprivation (OGD) model of neurons is an in vitro model of ischemia, hypoxia, and cognitive dysfunction.
Methods: We conducted clinical studies and in vitro experiments to investigate the clinical efficacy and mechanism of action of NBP for treating ACI-induced MCI. Patients with ACI-induced MCI were randomly divided into control (Ctrl) and NBP groups. We assessed various indicators, such as clinical efficacy, montreal cognitive assessment scale (MOCA), activities of daily living (ADL), and cerebral infarct size in both groups before and after treatment. We observed the morphology of neurons and detected the survival rate, action potentials (APs), expression of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), and the interaction between TLR4 and HMGB1.
Results: The MOCA and ADL scores increased significantly after treatment in the NBP group. A OGD model of neurons was established, and the neurons were divided into Ctrl and NBP groups. We observed that the survival rate and APs amplitude of the neurons were significantly increased in the NBP group, whereas TNF-α expression was decreased. Furthermore, the interaction between TLR4 and HMGB1 decreased in the NBP group.
Conclusion: NBP plays a neuroprotective role by inhibiting the TLR4/HMGB1 pathway and ameliorating ACI-induced MCI.
{"title":"A Preliminary Finding: N-butyl-phthalide Plays a Neuroprotective Role by Blocking the TLR4/HMGB1 Pathway and Improves Mild Cognitive Impairment Induced by Acute Cerebral Infarction.","authors":"Hong Zhou, Sijun Li, Cheng Huang, Yingping Chen, Liwen Wang, Junliang Lin, Yuan Lv","doi":"10.31083/j.jin2308158","DOIUrl":"10.31083/j.jin2308158","url":null,"abstract":"<p><strong>Background: </strong>Most acute cerebral infarctions (ACI) may develop vascular dementia (VD), which involves almost all types of cognitive impairment. Unfortunately, there is currently no effective treatment for VD. Most patients exhibit mild cognitive impairment (MCI) before the development of VD. N-butyl-phthalide (NBP) is used to treat ACI and improve cognitive function. The oxygen and glucose deprivation (OGD) model of neurons is an <i>in vitro</i> model of ischemia, hypoxia, and cognitive dysfunction.</p><p><strong>Methods: </strong>We conducted clinical studies and <i>in vitro</i> experiments to investigate the clinical efficacy and mechanism of action of NBP for treating ACI-induced MCI. Patients with ACI-induced MCI were randomly divided into control (Ctrl) and NBP groups. We assessed various indicators, such as clinical efficacy, montreal cognitive assessment scale (MOCA), activities of daily living (ADL), and cerebral infarct size in both groups before and after treatment. We observed the morphology of neurons and detected the survival rate, action potentials (APs), expression of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), and the interaction between TLR4 and HMGB1.</p><p><strong>Results: </strong>The MOCA and ADL scores increased significantly after treatment in the NBP group. A OGD model of neurons was established, and the neurons were divided into Ctrl and NBP groups. We observed that the survival rate and APs amplitude of the neurons were significantly increased in the NBP group, whereas TNF-α expression was decreased. Furthermore, the interaction between TLR4 and HMGB1 decreased in the NBP group.</p><p><strong>Conclusion: </strong>NBP plays a neuroprotective role by inhibiting the TLR4/HMGB1 pathway and ameliorating ACI-induced MCI.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"158"},"PeriodicalIF":2.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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