{"title":"Postnatal expression of Cat-315-positive perineuronal nets in the SAMP10 mouse primary somatosensory cortex","authors":"Hiroshi Ueno , Yu Takahashi , Sachiko Mori , Eriko Kitano , Shinji Murakami , Kenta Wani , Yosuke Matsumoto , Motoi Okamoto , Takeshi Ishihara","doi":"10.1016/j.ibneur.2025.01.012","DOIUrl":"10.1016/j.ibneur.2025.01.012","url":null,"abstract":"<div><div>Perineuronal nets (PNNs) form at the end of the critical period of plasticity in the mouse primary somatosensory cortex. PNNs are said to have functions that control neuroplasticity and provide neuroprotection. However, it is not clear which molecules in PNNs have these functions. We have previously reported that Cat-315-positive molecules were not expressed in the PNNs of the senescence-accelerated model (SAM)P10 strain model mice at 12 months of age. To confirm whether the loss of Cat-315-positive molecules occurred early in life in SAMP10 mice, we examined Cat-315-positive PNNs in the primary somatosensory cortex during postnatal development. This research helps to elucidate the function of PNNs and the mechanism of cognitive decline associated with ageing. To confirm whether Cat-315-positive PNNs changed in an age-dependent manner in SAMP10 mice, we examined the primary somatosensory cortex at 21, 28, and 56 days after birth. We compared these results with those of senescence-accelerated mouse-resistant (SAMR) mice. In SAMP10 mice, Cat-315-positive PNNs were expressed in the primary somatosensory cortex early after birth, but their expression was significantly lower than that in SAMR1 mice. Many other molecules that calibrated the PNN were unchanged between SAMP10 and SAMR1 mice. This study revealed that the expression of the Cat-315 epitope was decreased in the primary somatosensory cortex of SAMP10 mice during postnatal development. SAMP10 mice have had histological abnormalities in their brains since early life. Furthermore, using SAMP10 will be useful in elucidating the mechanism of age-related abnormalities in brain function as well as in elucidating the function and structure of PNNs.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 244-256"},"PeriodicalIF":2.0,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143093497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Association between periodontitis and Alzheimer's disease: A narrative review","authors":"Mohammad Amin Seyedmoalemi , Zahra Saied-Moallemi","doi":"10.1016/j.ibneur.2024.12.004","DOIUrl":"10.1016/j.ibneur.2024.12.004","url":null,"abstract":"<div><div>Periodontitis is a chronic inflammatory disease that progressively damages the supporting structures of teeth, resulting in gum bleeding, inflammation, gum recession, and eventual tooth loss. Key factors, including poor oral hygiene, plaque accumulation, smoking, inadequate nutrition, and genetic predisposition, drive its development. Recent evidence underscores the potential role of periodontitis as a contributing factor to systemic diseases, including Alzheimer's disease (AD). AD is a neurodegenerative disorder marked by memory loss, cognitive decline, and brain inflammation. Emerging clinical and experimental studies indicate that these two conditions share overlapping risk factors and may be interconnected. One notable finding is the detection of specific periodontal pathogens, such as <em>Porphyromonas gingivalis</em> (P. gingivalis), in the brains of individuals with AD. This suggests a possible link between chronic oral infections and neurodegeneration. These pathogens are believed to exacerbate neuroinflammatory processes by activating microglia and promoting systemic inflammation, which is central to AD pathogenesis. Further research is needed to clarify the biological mechanisms underlying this association. Targeted interventions that address periodontitis, such as anti-inflammatory therapies or treatments targeting specific pathogens like <em>P. gingivalis</em>, could potentially mitigate its impact on the onset and progression of AD, offering a novel avenue for prevention and management strategies.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 360-365"},"PeriodicalIF":2.0,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kunlin Guo , Lei Gao , Ping Li, Shanwu Feng, Liping Zhao, Xian Wang
{"title":"Allopregnanolone relieves paclitaxel induced mechanical hypersensitivity via inhibiting spinal cord PGE2-EP2 mediated microglia-neuron signaling","authors":"Kunlin Guo , Lei Gao , Ping Li, Shanwu Feng, Liping Zhao, Xian Wang","doi":"10.1016/j.ibneur.2025.01.011","DOIUrl":"10.1016/j.ibneur.2025.01.011","url":null,"abstract":"<div><div>Chemotherapy-induced neuropathic pain (CINP) is a serious adverse effect of commonly used chemotherapeutics. Neurosteroid allopregnanolone is suggested to modulate the expression of various receptors or enzymes that involved in pain perception, presenting an analgesic potential. Here, we investigated if allopregnanolone attenuates extracellular signal-regulated kinase (ERK) and its downstream prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) expression in the dorsal spinal cord concomitant with neuropathic pain relief in paclitaxel (PTX)-induced neuropathic pain model rats. The results showed PTX upregulated phosphorylated ERK (p-ERK), PGE<sub>2</sub> level, and PGE<sub>2</sub> receptor E-prostanoid 2 (EP2) expression in the spinal dorsal horn. Besides, p-ERK inhibitor PD98059 or microglia inhibitor minocycline reduced microglial activation, p-ERK expression, PGE<sub>2</sub> release, EP2 expression, and partially alleviated PTX-induced mechanical hypersensitivity. Further, allopregnanolone level in the dorsal spinal cord was observed to decrease in CINP rats, and intragastric administration of exogenous allopregnanolone dose-dependently alleviated PTX-induced mechanical hypersensitivity. Mechanistically, allopregnanolone dose-dependently alleviated PTX-induced microglial activation, p-ERK, PGE<sub>2</sub>, and EP2 upregulation, as well as cytokines expression in the dorsal spinal cord in CINP rats. Furthermore, subcutaneous injection of allopregnanolone synthesis inhibitor medroxyprogesterone could reduce endogenous allopregnanolone and block all effects of exogenous allopregnanolone in CINP rats. Taken together, these results suggest allopregnanolone presents an analgesic effect for PTX-induced mechanical hypersensitivity, partially via inhibiting the dorsal spinal cord PGE<sub>2</sub>-EP2 mediated microglia-neuron signaling.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 211-221"},"PeriodicalIF":2.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143093395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Min Ming , Long Chen , Jian Huang , Ying Huang , Jiali Yin
{"title":"Effect of perampanel in reducing depression in patients with focal epilepsy","authors":"Min Ming , Long Chen , Jian Huang , Ying Huang , Jiali Yin","doi":"10.1016/j.ibneur.2025.01.007","DOIUrl":"10.1016/j.ibneur.2025.01.007","url":null,"abstract":"<div><h3>Background</h3><div>High prevalence of depression is very common in epilepsy. This study aimed to discover the effect of perampanel on depression in patients with focal epilepsy.</div></div><div><h3>Methods</h3><div>This is a prospective observational study. We included a total of 68 patients with focal EP, which were treated with perampanel. We analyzed data before perampanel treatment and at 6 and 12 months of follow-up of the optimal dose. Using the Beck Depression Inventory-II (BDI-II) scale to evaluate depression, the Mini-Mental State Examination (MMSE) to assess the cognitive function, and the Quality of Life in Epilepsy-31 items (QOLIE-31) to estimate the quality of life of EP patients.</div></div><div><h3>Results</h3><div>The BDI-II score improved significantly compared to before treatment and at 6 and 12 months of follow-up (P < 0.001). The mean total QOLIE-31 score significantly increased from 82.9 ± 20.4 to 88.7 ± 21.2 at the 12-month follow-up (P < 0.001). In addition, seizure control was improved significantly at 12 months: 32.1 % of patients were seizure-free, and 73.2 % were responsive. Moreover, there was statistical relationship between improvement in depression and seizure control. The MMSE score was not different before and after treatment (P > 0.05). Multiple Regression Analysis was found that annual family income, etiology, the frequency of attacks in recent years, types of ASMs and the age were the influence factors of pirampanel in reducing depression (<em>P</em><0.05).</div></div><div><h3>Conclusion</h3><div>Perampanel reduced depression symptoms in patients with focal epilepsy, although the lack of a control group or the relatively small sample size.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 257-262"},"PeriodicalIF":2.0,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143093496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Junhua Li, Chenhao Tang, Longfei Yang, Chen Song, Yanbin Wang
{"title":"The effect of sacral nerve root magnetic stimulation on bladder urodynamics and M3 receptor expression in rats with neurogenic bladder","authors":"Junhua Li, Chenhao Tang, Longfei Yang, Chen Song, Yanbin Wang","doi":"10.1016/j.ibneur.2025.01.010","DOIUrl":"10.1016/j.ibneur.2025.01.010","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the effect of sacral nerve root magnetic stimulation(SMS) on bladder urodynamics and M3 receptor expression in rats with neurogenic bladder.</div></div><div><h3>Methods</h3><div>30 adult female SD rats were randomly divided into Normal Group, Model Group, and Magnetic Stimulation Group, with 10 rats in each group. The Model Group and Magnetic Stimulation Group used the spinal cord transtion method to establish the neurogenic bladder animal model. After successful modeling, the Magnetic Stimulation Group received magnetic stimulation treatment once per day for 8 consutive weeks. After 8 weeks, bladder urodynamics were measured under anesthesia, rats were sacrificed, and bladder detrusor muscle tissue was collected for histological and ultrastructural observation, and M3 receptor expression levels were measured.</div></div><div><h3>Results</h3><div>The maximum bladder capacity and bladder compliance in the Magnetic Stimulation Group were higher than those in the Model Group (all <em>P</em> < 0. 05), and the leak point pressure was lower than that in the Model Group (P < 0. 05); there were no significant differences between the Magnetic Stimulation Group and the Normal Group in these three parameters (all <em>P</em> > 0. 05). H&E staining of bladder detrusor muscle tissue in the Magnetic Stimulation Group revealed minimal neutrophil infiltration. Moreover, the morphology and arrangement of the mucosal epithelial cells were closer to those observed in the Normal Group when compared with the Model Group. Under transmission electron microscopy, detrusor muscle cells had a smooth surface, slightly widened intercellular spaces, relatively uniform arrangement, and relatively intact mitochondrial structure. The expression level of M3 receptors in the bladder detrusor muscle tissue of the Magnetic Stimulation Group was significantly higher than that in the Normal Group and the Model Group (all <em>P</em> < 0. 05); there was no significant difference between the Model Group and the Normal Group (<em>P</em> > 0. 05).</div></div><div><h3>Conclusion</h3><div>Sacral nerve root magnetic stimulation has a certain effect on improving bladder function in rats with neurogenic bladder, which may be related to the increased expression level of M3 receptors in the bladder detrusor muscle tissue.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 158-162"},"PeriodicalIF":2.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ying Wu , Chao Wang , Wei Qian , Lieju Wang , Lina Yu , Minming Zhang , Min Yan
{"title":"Default mode network-basal ganglia network connectivity predicts the transition to postherpetic neuralgia","authors":"Ying Wu , Chao Wang , Wei Qian , Lieju Wang , Lina Yu , Minming Zhang , Min Yan","doi":"10.1016/j.ibneur.2025.01.009","DOIUrl":"10.1016/j.ibneur.2025.01.009","url":null,"abstract":"<div><h3>Background</h3><div>Neuroimaging studies have revealed aberrant network functional connectivity in postherpetic neuralgia (PHN) patients. However, there is a lack of knowledge regarding the relationship between the brain network connectivity during the acute period and disease prognosis.</div></div><div><h3>Objective</h3><div>The purpose of this study was to detect characteristic network connectivity in the process of herpes zoster (HZ) pain chronification and to identify whether abnormal network connectivity in the acute period can predict the outcome of patients with HZ.</div></div><div><h3>Methods</h3><div>In this cross-sectional study, 31 patients with PHN, 33 with recuperation from herpes zoster (RHZ), and 28 with acute herpes zoster (AHZ) were recruited and underwent resting-state functional magnetic resonance imaging (fMRI). We investigated the differences in the connectivity of four resting-state networks (RSN) among the three groups. Receiver operating characteristic (ROC) curve analysis was performed to identify whether abnormal network connectivity in the acute period could predict the outcome of patients with HZ.</div></div><div><h3>Results</h3><div>First, we found within-basal ganglia network (BGN) and default mode network (DMN)-BGN connectivity differences, with PHN patients showing increased DMN-BGN connectivity compared to AHZ and RHZ patients, while RHZ patients showing increased within-BGN connectivity compared to AHZ and PHN patients. Moreover, DMN-BGN connectivity was associated with the ID pain score in patients with AHZ. Finally, the DMN-BGN connectivity of AHZ patients could predict the outcome of HZ patients with sensitivity and specificity of 77.8 % and 63.2 %, respectively.</div></div><div><h3>Conclusions</h3><div>Our results provide evidence that DMN-BGN connectivity during the acute period confers a risk for the development of chronic pain and can act as a neuroimaging biomarker to predict the outcome of patients with HZ.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 135-141"},"PeriodicalIF":2.0,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11783054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neuroprotective effects of empagliflozin against scopolamine-induced memory impairment and oxidative stress in rats","authors":"Mahdieh Anoush , Neda Taghaddosi , Zahra Bokaei Hosseini , Fatemeh Rahmati , Soroush Bijani , Ali Kalantari-Hesari , Mir-Jamal Hosseini","doi":"10.1016/j.ibneur.2025.01.008","DOIUrl":"10.1016/j.ibneur.2025.01.008","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is one of the most common age-related neurodegenerative disorders. The main medicinal theory for the management of AD belongs to the acetyl-cholinesterase-inhibition pathway and NMDA antagonism. Recent investigation proposed memory improvement by sodium-glucose co-transporter 2 (SGLT2) inhibitors which indicated to improve glycemic control in adults with type 2 diabetes mellitus. According to the lack of sufficient evidence about the efficacy of empagliflozin (EMPA) for memory improvement, in comparison with donepezil (DON), the present research was carried out in order to investigate this hypothesis towards scopolamine-induced neurotoxicity on experimental male Wistar rats. The animals divided into two sets, each included 4 groups: The first set of Healthy animals [Control, EMPA (4 or 10 mg/kg), DON (1 mg/kg)]. The second set of rat Alzheimer model, which received 2 mg/kg Scopolamine by intraperitoneal route for 10 days followed by other treatments [AD, AD+ EMPA (4 or 10 mg/kg) and AD+DON]. Normal rats and AD rats, with each group receiving different substances for 8 consecutive days and 24 h after the accomplishment of the drug administrations, the memory functions assessed through Morris water maze (MWM) paradigm. This task was followed by decapitation of rats in order to evaluate the biochemical oxidative stress parameters in brain tissue. Our data indicated that EMPA significantly improved animals' performance in the behavioral test with a significant decrease in oxidative stress and antioxidant imbalance. In addition, EMPA (4 mg/kg) significantly reduced both cellular malondialdehyde and protein carbonyl content while conversely increased the total reduced glutathione content. Besides, the levels of total as well as endogenous antioxidants in the ferric reducing antioxidant power assay reported to be augmented. It seems that EMPA significantly improved both cellular biochemical aspects and memory performance in animal models in accordance with histopathological assessments. Conclusively, 4 mg/kg EMPA demonstrated better results in all aspects that were evaluated during this research.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 163-170"},"PeriodicalIF":2.0,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lipidopathy disrupts peripheral and central amyloid clearance in Alzheimer's disease: Where are our knowledge","authors":"Shahram Darabi , Enam Alhagh Charkhat Gorgich , Fatemeh Moradi , Auob Rustamzadeh","doi":"10.1016/j.ibneur.2025.01.004","DOIUrl":"10.1016/j.ibneur.2025.01.004","url":null,"abstract":"<div><div>Amyloid-beta (Aβ) production is a normal physiological process, essential for neuronal function. However, an imbalance in Aβ production and clearance is the central pathological feature of Alzheimer’s disease (AD), leading to the accumulation of Aβ plaques in the brain. Low-density lipoprotein receptor-related protein 1 (LRP1) plays a critical role in both the central clearance of Aβ from the brain and its peripheral transport to visceral organs. Disruptions in these processes contribute to the accumulation of Aβ in the central nervous system (CNS) and the progression of AD. Recent research emphasizes the need for a broader focus on the systemic effects of organs outside the brain, particularly in the context of AD prevention and treatment. The contribution of peripheral systems, such as the liver, in Aβ clearance, is vital, given that Aβ levels in the plasma correlate closely with those in the brain. Consequently, targeting systemic processes, rather than focusing solely on the CNS, may offer promising therapeutic approaches. Furthermore, high-density lipoprotein (HDL) facilitates the formation of lipoprotein-amyloid complexes, which are important for Aβ transport and clearance, using proteins such as apolipoproteins E and J (ApoE and ApoJ) to form complexes that help manage Aβ accumulation. On the other hand, low-density lipoprotein (LDL) facilitates Aβ efflux from the brain by binding to LRP1, promoting its clearance. Given the relationship between lipid profiles and Aβ levels, along with lipid-modifying drugs, may be effective in managing Aβ accumulation and mitigating AD progression.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 191-199"},"PeriodicalIF":2.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143093397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Examining the therapeutic potential and side effects of calcium channel blockers in mortality and morbidity of patients with stroke: A systematic review of pre-clinical and clinical studies","authors":"Sevak Hatamian , Asad Abdi , Fatemeh Sadat Seyedi Asl , Armin Tafazolimoghadam , Arian Tavasol , Seyed Ali Mousavi Nejad , Reza Madadi , Zohre Tajabadi , Mina Dehghani , Najmeh Ahmadpoor , Mobina Fathi , Mohammadreza Hajiesmaeili , Navid Nooraei","doi":"10.1016/j.ibneur.2025.01.002","DOIUrl":"10.1016/j.ibneur.2025.01.002","url":null,"abstract":"<div><h3>Background</h3><div>Blood pressure control is one of the basic steps in preventing stroke and cerebrovascular events. Calcium channel blockers are the first-line drugs in hypertension control. On the other hand, the stroke recovery phase depends on activating calcium channels and N-methyl-D-aspartate (NMDA) receptors. Considering these issues, one of the interdisciplinary challenges of neurology and cardiology is the use of these drugs in hypertensive patients with cerebrovascular accident (CVA) risk and their uses after these events.</div></div><div><h3>Objectives</h3><div>This study's primary goal is to evaluate the effects of calcium channel blockers on reducing the risk, mortality, morbidity, and long-term outcomes of cerebrovascular events.</div></div><div><h3>Material and Methods</h3><div>We conducted this systematic literature review by searching PubMed, Scopus, and Google Scholar databases. Our inclusion criteria were randomized clinical trials, cohort studies, case-cross-over studies, case reports, and in-vitro and animal studies in which they evaluated the effects of calcium channel blockers on the CVA risk and mortality, morbidity, and long-term outcomes of stroke. Our exclusion criteria were review studies with no adequate data and non-English articles. Articles that met our criteria were included in the initial search. After the title and abstract screening, 56 human and animal studies were selected to be discussed in this article.</div></div><div><h3>Results</h3><div>Among 56 selected studies, 33 were human studies, 23 were animal experiments, and one study was carried out both on animals and humans. A total of 1,860,234 patients were enrolled in 24 human studies. A total of 717,131 patients in 22 studies received CCBs. Two studies did not report the number of patients who underwent treatment with CCBs. Among 24 studies, 11 reported favorable outcomes following CCB administration, and two studies reported neuroprotective effects for CCBs without any adverse outcome in stroke patients. Five studies demonstrated that CCBs were associated with adverse outcomes. One study showed favorable and unfavorable outcomes compared to other antihypertensive agents. Stroke was reported in two studies following CCB overdose. Three studies have reported that CCBs had no significant effect on stroke risk, mortality, or long-term outcomes. In animal studies, a total of 813 animals were enrolled in 19 studies. Two studies were in vitro using mammalian cells and enzymes, and one study was ex-vivo. Among 24 studies, 18 (75 %) reported beneficial outcomes following treatment with CCBs, three (12.5 %) revealed both favorable and unfavorable results, two (8.3 %) demonstrated adverse outcomes, and one (4.2 %) showed no effect.</div></div><div><h3>Conclusion</h3><div>Based on the evidence from human and animal studies, authors conclude that CCBs are associated with a lower risk of stroke, lower mortality risk, and improved long-term neurological and ","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 222-243"},"PeriodicalIF":2.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143093498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Multimodal magnetic resonance imaging studies on non-motor symptoms of Parkinson's disease","authors":"Weimin Qi , Xiaoyan Niu , Xiuping Zhan, Yazhou Ren, Jianhang He, Jianxia Li, Xiaolin Hou, Haining Li","doi":"10.1016/j.ibneur.2025.01.003","DOIUrl":"10.1016/j.ibneur.2025.01.003","url":null,"abstract":"<div><h3>Objective</h3><div>This study aims to investigate the diagnostic value of multi-modal magnetic resonance imaging (MRI) utilizing arterial spin labeling (ASL), quantitative susceptibility mapping (QSM), and 3D T1-weighted imaging (3DT1WI) in patients with Parkinson's disease (PD). Additionally, it evaluates the relationship between MRI findings and non-motor symptoms associated with PD.</div></div><div><h3>Methods</h3><div>ASL, QSM, and 3DT1WI scans were performed on 48 PD patients and 46 healthy controls (HC). We extracted and analyzed differences in regional cerebral blood flow (rCBF), magnetic susceptibility, and gray matter density parameters between the two groups. These MRI parameters were correlated with clinical scale scores assessing non-motor symptoms, including cognitive function, sleep quality, olfaction, autonomic function, anxiety, depression, and fatigue. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic accuracy of each imaging modality in distinguishing PD from HC.</div></div><div><h3>Results</h3><div>The areas under the ROC curve (AUC) for rCBF, magnetic susceptibility, and gray matter density were 0.941, 0.979, and 0.624, respectively. In PD patients, a negative correlation was found between Unified Parkinson's Disease Rating Scale Part II (UPDRS II) scores and rCBF in the bilateral precuneus. The Pittsburgh Sleep Quality Index (PSQI) scores negatively correlated with rCBF in the left middle temporal gyrus and right middle occipital gyrus. Hamilton Depression Rating Scale (HAMD) scores positively correlated with QSM values in the right supplementary motor area, while scores on the Argentine Smell Identification Test (AHRS) negatively correlated with QSM values in the same area. Disease duration showed a positive correlation with QSM values in the right middle cingulate gyrus. Additionally, PSQI scores positively correlated with QSM values in the left middle cingulate gyrus, and fatigue severity scale (FSS) scores also positively correlated with QSM values in the left middle cingulate gyrus. Gray matter atrophy in the left inferior temporal gyrus was associated with cognitive impairment in PD.</div></div><div><h3>Conclusion</h3><div>Occipital hypoperfusion and cortical atrophy in the left inferior temporal gyrus may serve as novel imaging biomarkers for PD and are associated with sleep disturbances and cognitive impairment in PD patients. Extensive iron deposition in the bilateral cerebral cortex of PD patients may be a contributing factor to non-motor symptoms such as sleep disturbances and fatigue. Multimodal imaging techniques, including ASL, QSM, and 3DT1WI, can enhance the diagnostic accuracy for PD.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 180-190"},"PeriodicalIF":2.0,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}