Pub Date : 2024-09-29DOI: 10.1016/j.neulet.2024.138001
Elvis Cuevas, Susan Lantz, Glenn Newport, Becky Divine, Qiangen Wu, Merle G Paule, J César Tobón-Velasco, Syed F Ali, Abel Santamaría
{"title":"Retraction notice to \"On the early toxic effect of quinolinic acid: Involvement of RAGE\" [Neurosci. Lett. 474(2) (2010) 74-78].","authors":"Elvis Cuevas, Susan Lantz, Glenn Newport, Becky Divine, Qiangen Wu, Merle G Paule, J César Tobón-Velasco, Syed F Ali, Abel Santamaría","doi":"10.1016/j.neulet.2024.138001","DOIUrl":"https://doi.org/10.1016/j.neulet.2024.138001","url":null,"abstract":"","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350911","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}
Pub Date : 2024-09-27DOI: 10.1016/j.neulet.2024.137998
Baris Metin, Secil Damla Kayaalp, Shams Farhad, Elvan Ciftci, Buse Gocmen Er, Nevzat Tarhan
Recent studies have prompted a shift in the understanding of attention deficit hyperactivity disorder (ADHD) from models positing dysfunction of individual brain areas to those that assume alterations in large-scale brain networks. Despite this shift, the underlying neural mechanism of ADHD in the adult population remains uncertain. With functional magnetic resonance imaging (fMRI), this study examined brain connectivity of dorsal and ventral attention networks. Adults with and without ADHD completed a Go/No-Go task inside the scanner and the functional connectivity of attention networks was analysed. The generalized psychophysiological interaction analysis indicated differences involving the dorsal attention network. For the ADHD group, an interaction effect revealed altered dorsal attention-default mode network connectivity modulation, particularly between the right frontal eye field and posterior cingulate gyrus. We conclude that dorsal attention network dysfunction may be involved in sustained attention deficits in adult-ADHD. This study sheds light into network-level alterations contributing to the understanding of adult-ADHD, which may be a potential avenue for future research and clinical interventions.
{"title":"Task-based modulation of functional connectivity of dorsal attention network in adult-ADHD.","authors":"Baris Metin, Secil Damla Kayaalp, Shams Farhad, Elvan Ciftci, Buse Gocmen Er, Nevzat Tarhan","doi":"10.1016/j.neulet.2024.137998","DOIUrl":"https://doi.org/10.1016/j.neulet.2024.137998","url":null,"abstract":"<p><p>Recent studies have prompted a shift in the understanding of attention deficit hyperactivity disorder (ADHD) from models positing dysfunction of individual brain areas to those that assume alterations in large-scale brain networks. Despite this shift, the underlying neural mechanism of ADHD in the adult population remains uncertain. With functional magnetic resonance imaging (fMRI), this study examined brain connectivity of dorsal and ventral attention networks. Adults with and without ADHD completed a Go/No-Go task inside the scanner and the functional connectivity of attention networks was analysed. The generalized psychophysiological interaction analysis indicated differences involving the dorsal attention network. For the ADHD group, an interaction effect revealed altered dorsal attention-default mode network connectivity modulation, particularly between the right frontal eye field and posterior cingulate gyrus. We conclude that dorsal attention network dysfunction may be involved in sustained attention deficits in adult-ADHD. This study sheds light into network-level alterations contributing to the understanding of adult-ADHD, which may be a potential avenue for future research and clinical interventions.</p>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350912","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}
Pub Date : 2024-09-26DOI: 10.1016/j.neulet.2024.138004
Background
It has been established that there are functional changes in the brain of treatment-resistant depression (TRD) patients, but previous studies of functional connectivity (FC) usually involved selection of regions of interest based on accumulated a priori knowledge of the disorder. In this study, we combine amplitude of low-frequency fluctuation (ALFF) and FC; this approach, based on the abnormal ALFF, may provide some insights into the neural basis of the disease in terms of fMRI signals of low-frequency fluctuations.
Methods
A total of 16 TRD patients, who visited the Qingdao Mental Health Center, Shandong Province, China between March 2023 and January 2024, along with 16 normal subjects, were enrolled into this study for functional imaging. In this study, we first explored the ALFF changes of TRD patients at a baseline resting state. Second, we selected the regions that were significantly changed in the ALFF as seeds and calculated the regional activity and functional connectivity (FC) of these regions using a seed-based approach. We also calculated correlations between the percent change in the PDQ-5D scores and ALFF values in brain regions with differing activity for TRD patients.
Results
During the baseline resting state, by using the ALFF, we found a significantly decreased or increased ALFF in the TRD patients relative to the controls. These regions were located in the left/right postcentral gyrus (PoCG.L/PoCG.R), right cuneus(CUN.R). We found that the ALFF values of the right hippocampus (HIP.R) in the TRD group were negatively correlated with the PDQ-5D score. Then, we selected these brain regions as seeds to investigate the FC changes in brains of TRD patients. We found abnormal functional connectivity in left/right middle frontal gyrus(MFG.L/MFG.R), the right Inferior frontal gyrus, opercular part (IFGoperc.R), the left/right Anterior cingulate and paracingulate gyri (ACC.L/ACC.R), the right supramarginal gyrus (SMG.R), and the right Calcarine fissure and surrounding cortex (CAL.R).
Conclusion
We found a larger range of altered brain regions in TRD patients compared to healthy controls, especially in the central executive network (CEN), salience network (SN) and default mode network (DMN).
{"title":"Altered brain function in treatment-resistant depression patients: A resting-state functional magnetic resonance imaging study","authors":"","doi":"10.1016/j.neulet.2024.138004","DOIUrl":"10.1016/j.neulet.2024.138004","url":null,"abstract":"<div><h3>Background</h3><div>It has been established that there are functional changes in the brain of treatment-resistant depression (TRD) patients, but previous studies of functional connectivity (FC) usually involved selection of regions of interest based on accumulated a priori knowledge of the disorder. In this study, we combine amplitude of low-frequency fluctuation (ALFF) and FC; this approach, based on the abnormal ALFF, may provide some insights into the neural basis of the disease in terms of fMRI signals of low-frequency fluctuations.</div></div><div><h3>Methods</h3><div>A total of 16 TRD patients, who visited the Qingdao Mental Health Center, Shandong Province, China between March 2023 and January 2024, along with 16 normal subjects, were enrolled into this study for functional imaging. In this study, we first explored the ALFF changes of TRD patients at a baseline resting state. Second, we selected the regions that were significantly changed in the ALFF as seeds and calculated the regional activity and functional connectivity (FC) of these regions using a seed-based approach. We also calculated correlations between the percent change in the PDQ-5D scores and ALFF values in brain regions with differing activity for TRD patients.</div></div><div><h3>Results</h3><div>During the baseline resting state, by using the ALFF, we found a significantly decreased or increased ALFF in the TRD patients relative to the controls. These regions were located in the left/right postcentral gyrus (PoCG.L/PoCG.R), right cuneus(CUN.R). We found that the ALFF values of the right hippocampus (HIP.R) in the TRD group were negatively correlated with the PDQ-5D score. Then, we selected these brain regions as seeds to investigate the FC changes in brains of TRD patients. We found abnormal functional connectivity in left/right middle frontal gyrus(MFG.L/MFG.R), the right Inferior frontal gyrus, opercular part (IFGoperc.R), the left/right Anterior cingulate and paracingulate gyri (ACC.L/ACC.R), the right supramarginal gyrus (SMG.R), and the right Calcarine fissure and surrounding cortex (CAL.R).</div></div><div><h3>Conclusion</h3><div>We found a larger range of altered brain regions in TRD patients compared to healthy controls, especially in the central executive network (CEN), salience network (SN) and default mode network (DMN).</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26DOI: 10.1016/j.neulet.2024.138003
Peripheral neuropathy, resulting from damage to peripheral nerves, manifests as weakness, numbness, and pain, primarily affecting extremities and significantly impairing quality of life, especially in the elderly. Current treatments often entail severe side effects, necessitating the exploration of alternative therapies. Harmaline, a β-carboline alkaloid derived from Peganum harmala, exhibits promising antioxidant and anti-inflammatory properties. This study aimed to assess the efficacy of harmaline in a vincristine-induced mouse model of peripheral neuropathy. Swiss albino mice received vincristine (0.1 mg/kg, i.p.) for 10 days to induce neuropathy. Harmaline (5 and 10 mg/kg, i.p.) was administered 30 min before vincristine and continued until day 14 to evaluate its protective effects. Behavioral assessments were conducted on days 7 and 14. Vincristine treatment significantly heightened sensitivity to cold, measured by cold plate and acetone drop tests, and to heat, assessed via the hot plate test, while also impairing motor coordination. Biochemical analyses revealed decreased levels of GSH and Nrf-2, alongside elevated TBARS and IL-1β levels in sciatic nerve tissue. Harmaline administration markedly alleviated both behavioral and biochemical alterations induced by vincristine, with the 10 mg/kg dose exhibiting the most pronounced effects. Notably, harmaline treatment elevated GSH and Nrf-2 levels while reducing TBARS and IL-1β. Furthermore, substance-P treatment reversed the protective effects of harmaline, implicating the NK-1 receptor in its mechanism of action. In conclusion, harmaline demonstrates significant potential in mitigating vincristine-induced peripheral neuropathy by reducing oxidative stress through Nrf-2 activation and lowering IL-1β levels, likely via NK-1 receptor inhibition.
{"title":"Harmaline attenuates chemotherapy-induced peripheral neuropathy: Modulation of Nrf-2 pathway and NK-1 receptor signaling","authors":"","doi":"10.1016/j.neulet.2024.138003","DOIUrl":"10.1016/j.neulet.2024.138003","url":null,"abstract":"<div><div>Peripheral neuropathy, resulting from damage to peripheral nerves, manifests as weakness, numbness, and pain, primarily affecting extremities and significantly impairing quality of life, especially in the elderly. Current treatments often entail severe side effects, necessitating the exploration of alternative therapies. Harmaline, a β-carboline alkaloid derived from <em>Peganum harmala</em>, exhibits promising antioxidant and anti-inflammatory properties. This study aimed to assess the efficacy of harmaline in a vincristine-induced mouse model of peripheral neuropathy. Swiss albino mice received vincristine (0.1 mg/kg, i.p.) for 10 days to induce neuropathy. Harmaline (5 and 10 mg/kg, i.p.) was administered 30 min before vincristine and continued until day 14 to evaluate its protective effects. Behavioral assessments were conducted on days 7 and 14. Vincristine treatment significantly heightened sensitivity to cold, measured by cold plate and acetone drop tests, and to heat, assessed via the hot plate test, while also impairing motor coordination. Biochemical analyses revealed decreased levels of GSH and Nrf-2, alongside elevated TBARS and IL-1β levels in sciatic nerve tissue. Harmaline administration markedly alleviated both behavioral and biochemical alterations induced by vincristine, with the 10 mg/kg dose exhibiting the most pronounced effects. Notably, harmaline treatment elevated GSH and Nrf-2 levels while reducing TBARS and IL-1β. Furthermore, substance-P treatment reversed the protective effects of harmaline, implicating the NK-1 receptor in its mechanism of action. In conclusion, harmaline demonstrates significant potential in mitigating vincristine-induced peripheral neuropathy by reducing oxidative stress through Nrf-2 activation and lowering IL-1β levels, likely via NK-1 receptor inhibition.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350913","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}
Pub Date : 2024-09-24DOI: 10.1016/j.neulet.2024.137997
Visual system is the most important system of animal to cognize the information in outside world, and reward-related visual cues are the key factors in the consolidation and retrieval of reward memory. However, the neural circuit mechanism is still unclear. Superior Colliculus (SC) receive direct input from the retina and belong to the earliest stages of visual processing. Recent studies identified a specific pathway from SC to ventral tegmental area (VTA) that underlie specific innate behaviors, eg. flight or freezing, approach behaviors and so on. In present research, we investigated that inhibition of SC to VTA circuit with chemogenetics suppressed light cue-associated reward-seeking behaviors, while activation of the SC-VTA circuit with chemogenetic technology triggered the reward-seeking behaviors in optical intracranial self-stimulation for VTA DA neurons (oICSS) in mice. These findings suggest that neural circuit of SC-VTA mediates the retrieval of reward memory associated with visual cues, which will provide a new field for revealing the neural mechanism of pathological memory such as addiction.
{"title":"The neural circuit of Superior colliculus to ventral tegmental area modulates visual cue associated with rewarding behavior in optical intracranial Self-Stimulation in mice","authors":"","doi":"10.1016/j.neulet.2024.137997","DOIUrl":"10.1016/j.neulet.2024.137997","url":null,"abstract":"<div><div>Visual system is the most important system of animal to cognize the information in outside world, and reward-related visual cues are the key factors in the consolidation and retrieval of reward memory. However, the neural circuit mechanism is still unclear. Superior Colliculus (SC) receive direct input from the retina and belong to the earliest stages of visual processing. Recent studies identified a specific pathway from SC to ventral tegmental area (VTA) that underlie specific innate behaviors, eg. flight or freezing, approach behaviors and so on. In present research, we investigated that inhibition of SC to VTA circuit with chemogenetics suppressed light cue-associated reward-seeking behaviors, while activation of the SC-VTA circuit with chemogenetic technology triggered the reward-seeking behaviors in optical intracranial self-stimulation for VTA DA neurons (oICSS) in mice. These findings suggest that neural circuit of SC-VTA mediates the retrieval of reward memory associated with visual cues, which will provide a new field for revealing the neural mechanism of pathological memory such as addiction.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350914","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}
Pub Date : 2024-09-22DOI: 10.1016/j.neulet.2024.137991
Dopamine (DA) is a catecholamine neurotransmitter that works to regulate cognitive functions. Patients affected by Parkinson’s Disease (PD) experience a loss of dopaminergic neurons and downregulated neural DA production. This leads to cognitive and physical decline that is the hallmark of PD for which no cure currently exists. Danio rerio, or zebrafish, have become an increasingly popular disease model used in PD pharmaceutical development. This model still requires extensive development to better characterize which PD features are adequately represented. Furthermore, the great majority of PD zebrafish models have been performed in embryos, which may not be relevant towards age-related human PD. As an improvement, mature D. rerio were treated with neurotoxic prodrug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) through intraperitoneal injection to induce parkinsonism. Behavioral analysis confirmed disparities in movement between saline-injected control and the MPTP-injected experimental group, with swim distance and speed significantly lowered seven days after MPTP injection. Simultaneously, cognitive decline was apparent in MPTP-injected zebrafish, demonstrated by decreased alternation in a y-maze. RT-qPCR confirmed trends consistent with downregulation in Parkinsonian genetic markers, specifically DA transporter (DAT), MAO-B, PINK1. In summary, mature zebrafish injected with MPTP present with similar movement and cognitive decline as compared to human disease. Despite its benefits, this model does not appear to recapitulate pathophysiology of the disease with the full profile of expected gene downregulation. Because of this, it is important that researchers looking for pharmacological interventions for PD only use this zebrafish model when targeting the human-relevant PD symptoms and causes that are represented.
多巴胺（DA）是一种儿茶酚胺神经递质，可调节认知功能。帕金森病（PD）患者会丧失多巴胺能神经元，神经系统分泌的多巴胺也会减少。这导致认知能力和身体机能下降，是帕金森病的特征，目前尚无治疗方法。Danio rerio（斑马鱼）已成为一种越来越流行的疾病模型，用于帕金森病的药物开发。这一模型仍需要广泛的开发，以更好地确定哪些帕金森病特征得到了充分体现。此外，绝大多数帕金森病斑马鱼模型都是在胚胎中进行的，这可能与年龄相关的人类帕金森病无关。作为一种改进，通过腹腔注射神经毒性原药 1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）来诱导帕金森氏症，对成熟的 D. rerio 进行了处理。行为分析证实，注射生理盐水的对照组和注射 MPTP 的实验组在运动方面存在差异，注射 MPTP 七天后，游泳距离和速度明显降低。同时，注射 MPTP 的斑马鱼的认知能力明显下降，表现为在 y 型迷宫中的交替能力下降。RT-qPCR 证实了与帕金森病遗传标记下调一致的趋势，特别是 DA 转运体 (DAT)、MAO-B 和 PINK1。总之，注射 MPTP 的成熟斑马鱼的运动和认知能力下降与人类疾病相似。尽管该模型有其优点，但它似乎并不能再现该疾病的病理生理学，也不能再现预期基因下调的全貌。因此，研究人员在寻找治疗帕金森氏症的药物干预措施时，只有在针对与人类相关的帕金森氏症症状和病因时才使用这种斑马鱼模型，这一点非常重要。
{"title":"1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated adult zebrafish as a model for Parkinson’s Disease","authors":"","doi":"10.1016/j.neulet.2024.137991","DOIUrl":"10.1016/j.neulet.2024.137991","url":null,"abstract":"<div><div>Dopamine (DA) is a catecholamine neurotransmitter that works to regulate cognitive functions. Patients affected by Parkinson’s Disease (PD) experience a loss of dopaminergic neurons and downregulated neural DA production. This leads to cognitive and physical decline that is the hallmark of PD for which no cure currently exists. <em>Danio rerio</em>, or zebrafish, have become an increasingly popular disease model used in PD pharmaceutical development. This model still requires extensive development to better characterize which PD features are adequately represented. Furthermore, the great majority of PD zebrafish models have been performed in embryos, which may not be relevant towards age-related human PD. As an improvement, mature <em>D. rerio</em> were treated with neurotoxic prodrug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) through intraperitoneal injection to induce parkinsonism. Behavioral analysis confirmed disparities in movement between saline-injected control and the MPTP-injected experimental group, with swim distance and speed significantly lowered seven days after MPTP injection. Simultaneously, cognitive decline was apparent in MPTP-injected zebrafish, demonstrated by decreased alternation in a y-maze. RT-qPCR confirmed trends consistent with downregulation in Parkinsonian genetic markers, specifically DA transporter (DAT), MAO-B, PINK1. In summary, mature zebrafish injected with MPTP present with similar movement and cognitive decline as compared to human disease. Despite its benefits, this model does not appear to recapitulate pathophysiology of the disease with the full profile of expected gene downregulation. Because of this, it is important that researchers looking for pharmacological interventions for PD only use this zebrafish model when targeting the human-relevant PD symptoms and causes that are represented.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142323320","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}
Pub Date : 2024-09-21DOI: 10.1016/j.neulet.2024.137995
Alpha-synuclein deposits in the brain have been suspected to cause Parkinson’s disease and dementia with Lewy bodies (DLB). It was recently revealed that the glymphatic system is largely responsible for the removal of alpha-synuclein. We investigated changes in the glymphatic system’s activity by determining the DTI‑ALPS (diffusion tensor image analysis along the perivascular space) index in DLB patients. Twenty-six patients with DLB and 43 healthy subjects underwent diffusion tensor imaging (DTI) scanning at our hospital during the period April 2013 to March 2023. We retrospectively computed each subject’s DTI‑ALPS index to evaluate his/her glymphatic-system activity and then analyzed the relationships between the subjects’ DTI‑ALPS index data and their DLB neuroimaging biomarker values. A significant reduction of the DTI‑ALPS index was observed in the patients with DLB compared to the healthy subjects. Significant positive correlations were also detected in the DLB group between the DTI‑ALPS index and the regional gray matter volume in the left insula and between the index and the specific binding ratio of 123I–N-ω-fluoropropyl-2β-carboxymethoxy-3β-(4-iodophenyl)nortropane ([123I]-FP-CIT). These results indicate that (i) the DTI‑ALPS index is a good biomarker of the progression of DLB, and (ii) this index might be effective to distinguish DLB from other neurocognitive disorders.
{"title":"Relationships between neuroimaging biomarkers and glymphatic-system activity in dementia with Lewy bodies","authors":"","doi":"10.1016/j.neulet.2024.137995","DOIUrl":"10.1016/j.neulet.2024.137995","url":null,"abstract":"<div><div>Alpha-synuclein deposits in the brain have been suspected to cause Parkinson’s disease and dementia with Lewy bodies (DLB). It was recently revealed that the glymphatic system is largely responsible for the removal of alpha-synuclein. We investigated changes in the glymphatic system’s activity by determining the DTI‑ALPS (diffusion tensor image analysis along the perivascular space) index in DLB patients. Twenty-six patients with DLB and 43 healthy subjects underwent diffusion tensor imaging (DTI) scanning at our hospital during the period April 2013 to March 2023. We retrospectively computed each subject’s DTI‑ALPS index to evaluate his/her glymphatic-system activity and then analyzed the relationships between the subjects’ DTI‑ALPS index data and their DLB neuroimaging biomarker values. A significant reduction of the DTI‑ALPS index was observed in the patients with DLB compared to the healthy subjects. Significant positive correlations were also detected in the DLB group between the DTI‑ALPS index and the regional gray matter volume in the left insula and between the index and the specific binding ratio of <sup>123</sup>I–N-ω-fluoropropyl-2β-carboxymethoxy-3β-(4-iodophenyl)nortropane ([<sup>123</sup>I]-FP-CIT). These results indicate that (<em>i</em>) the DTI‑ALPS index is a good biomarker of the progression of DLB, and (<em>ii</em>) this index might be effective to distinguish DLB from other neurocognitive disorders.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292256","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}
Pub Date : 2024-09-20DOI: 10.1016/j.neulet.2024.137994
This study aimed to explore the potential antiallodynic effects of rosmarinic acid, a natural antioxidant with a demonstrated safety profile across a broad dose range. Using a chronic constriction injury-induced neuropathic pain model, the impact of rosmarinic acid on allodynia was investigated. Furthermore, the involvement of adrenergic and opioidergic mechanisms in its activity was assessed. To evaluate rosmarinic acid’s efficacy, doses of 10, 20, and 40 mg/kg were administered and the electronic von Frey test was utilized along with an activity cage apparatus. % MPE values were calculated to gauge the extent of pain relief. Mechanistic insights were obtained by pretreating animals with the β-adrenergic receptor antagonist propranolol, the α1-adrenergic receptor antagonist prazosin, α2-adrenergic receptor antagonist yohimbine, and the opioid receptor antagonist naloxone. Rosmarinic acid demonstrated a statistically significant antiallodynic effect that was independent of locomotor activity. This effect was noteworthy as it resembled both the level and duration of relief provided by pregabalin. Additionally, the %MPE value of the group treated with 40 mg/kg rosmarinic acid showed a significant difference compared to the value of the pregabalin-treated group (P<0.001). Pre-administration of the antagonists revealed that the antiallodynic activity was shown to be mediated by the stimulation of opioid and adrenergic receptors, with a primary contribution from α2-adrenergic receptor stimulation. Our findings suggest that rosmarinic acid may hold promise as a potential therapeutic agent for neuropathic pain. By elucidating the involvement of adrenergic and opioidergic mechanisms, we have provided valuable preclinical data that could inform novel treatment approaches.
{"title":"Examination of the antiallodynic effect of rosmarinic acid in neuropathic pain and possible mechanisms of action","authors":"","doi":"10.1016/j.neulet.2024.137994","DOIUrl":"10.1016/j.neulet.2024.137994","url":null,"abstract":"<div><div>This study aimed to explore the potential antiallodynic effects of rosmarinic acid, a natural antioxidant with a demonstrated safety profile across a broad dose range. Using a chronic constriction injury-induced neuropathic pain model, the impact of rosmarinic acid on allodynia was investigated. Furthermore, the involvement of adrenergic and opioidergic mechanisms in its activity was assessed. To evaluate rosmarinic acid’s efficacy, doses of 10, 20, and 40 mg/kg were administered and the electronic von Frey test was utilized along with an activity cage apparatus. % MPE values were calculated to gauge the extent of pain relief. Mechanistic insights were obtained by pretreating animals with the β-adrenergic receptor antagonist propranolol, the α1-adrenergic receptor antagonist prazosin, α2-adrenergic receptor antagonist yohimbine, and the opioid receptor antagonist naloxone. Rosmarinic acid demonstrated a statistically significant antiallodynic effect that was independent of locomotor activity. This effect was noteworthy as it resembled both the level and duration of relief provided by pregabalin. Additionally, the %MPE value of the group treated with 40 mg/kg rosmarinic acid showed a significant difference compared to the value of the pregabalin-treated group (P<0.001). Pre-administration of the antagonists revealed that the antiallodynic activity was shown to be mediated by the stimulation of opioid and adrenergic receptors, with a primary contribution from α2-adrenergic receptor stimulation. Our findings suggest that rosmarinic acid may hold promise as a potential therapeutic agent for neuropathic pain. By elucidating the involvement of adrenergic and opioidergic mechanisms, we have provided valuable preclinical data that could inform novel treatment approaches.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292294","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}
Pub Date : 2024-09-19DOI: 10.1016/j.neulet.2024.137993
It is known that exercise increases brain-derived neurotrophic factor (BDNF) levels in the hippocampus, the brain region responsible for learning and memory, resulting in improved cognitive functions and learning processes. However, it is claimed that different types of exercise cause different responses in the brain. It is thought that lactate and osteocalcin secreted in response to exercise are associated with an increase in BDNF levels. However, there are not enough studies on this subject. This study aimed to compare the effects of high-intensity interval training (HIIT) and voluntary exercise training on cognitive performance and molecular connections. Male rats were randomly divided into control, voluntary exercise training and HIIT groups. The voluntary exercise group had free access to the voluntary wheel for 8 weeks. The HIIT group performed HIIT on the treadmill 3 days a week for 8 weeks. The rats underwent open field (OF), elevated plus maze (EPM) and Morris water maze (MWM) tests 24 h after the last exercise training. Then, after blood was drawn under anesthesia, the rats were sacrificed and their hippocampus tissues were separated. Glucocorticoid and BDNF levels in the blood were evaluated by enzyme-linked immunosorbent assay (ELISA), and osteocalcin and BDNF expressions in the hippocampus were evaluated by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). Neither voluntary exercise training nor HIIT had any significant effect on behavioral parameters assessed by OF, EPM and MWM tests. However, BDNF expression in hippocampus tissue was higher in the HIIT group than in the control group. In addition, osteocalcin expression in hippocampus tissue was higher in the HIIT and voluntary exercise groups than in the control group. In conclusion, according to the findings we obtained from this study, although it does not have a significant effect on cognitive functions, the effect of HIIT on brain functions seems to be more effective than voluntary exercise.
{"title":"Comparing the effect of high-intensity interval exercise and voluntary exercise training on cognitive functions in rats","authors":"","doi":"10.1016/j.neulet.2024.137993","DOIUrl":"10.1016/j.neulet.2024.137993","url":null,"abstract":"<div><div>It is known that exercise increases brain-derived neurotrophic factor (BDNF) levels in the hippocampus, the brain region responsible for learning and memory, resulting in improved cognitive functions and learning processes. However, it is claimed that different types of exercise cause different responses in the brain. It is thought that lactate and osteocalcin secreted in response to exercise are associated with an increase in BDNF levels. However, there are not enough studies on this subject. This study aimed to compare the effects of high-intensity interval training (HIIT) and voluntary exercise training on cognitive performance and molecular connections. Male rats were randomly divided into control, voluntary exercise training and HIIT groups. The voluntary exercise group had free access to the voluntary wheel for 8 weeks. The HIIT group performed HIIT on the treadmill 3 days a week for 8 weeks. The rats underwent open field (OF), elevated plus maze (EPM) and Morris water maze (MWM) tests 24 h after the last exercise training. Then, after blood was drawn under anesthesia, the rats were sacrificed and their hippocampus tissues were separated. Glucocorticoid and BDNF levels in the blood were evaluated by enzyme-linked immunosorbent assay (ELISA), and osteocalcin and BDNF expressions in the hippocampus were evaluated by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). Neither voluntary exercise training nor HIIT had any significant effect on behavioral parameters assessed by OF, EPM and MWM tests. However, BDNF expression in hippocampus tissue was higher in the HIIT group than in the control group. In addition, osteocalcin expression in hippocampus tissue was higher in the HIIT and voluntary exercise groups than in the control group. In conclusion, according to the findings we obtained from this study, although it does not have a significant effect on cognitive functions, the effect of HIIT on brain functions seems to be more effective than voluntary exercise.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292293","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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