Neural Plasticity最新文献_第4页

Fractalkine/CX3CR1-Dependent Modulation of Synaptic and Network Plasticity in Health and Disease. Fractalkine/ cx3cr1依赖性突触和网络可塑性在健康和疾病中的调节。

IF 3.1 4区医学

Neural Plasticity Pub Date : 2023-01-01 DOI: 10.1155/2023/4637073

N P Camacho-Hernández, F Peña-Ortega

引用次数: 2

Astragaloside IV Alleviates Brain Injury Induced by Hypoxia via the Calpain-1 Signaling Pathway. 黄芪皂苷 IV 通过钙蛋白酶-1 信号通路缓解缺氧引起的脑损伤

IF 3 4区医学

Neural Plasticity Pub Date : 2022-12-03 eCollection Date: 2022-01-01 DOI: 10.1155/2022/6509981

Yan Meng, Shengxue Yu, Fang Zhao, Yu Liu, Yue Wang, Siqi Fan, Yuhong Su, Meili Lu, Hongxin Wang

{"title":"Astragaloside IV Alleviates Brain Injury Induced by Hypoxia via the Calpain-1 Signaling Pathway.","authors":"Yan Meng, Shengxue Yu, Fang Zhao, Yu Liu, Yue Wang, Siqi Fan, Yuhong Su, Meili Lu, Hongxin Wang","doi":"10.1155/2022/6509981","DOIUrl":"10.1155/2022/6509981","url":null,"abstract":"Long-term hypoxia can induce oxidative stress and apoptosis in hippocampal neurons that can lead to brain injury diseases. Astragaloside IV (AS-IV) is widely used in the antiapoptotic therapy of brain injury diseases. However, its mechanism of action is still not fully understood. In this study, we investigated the effect of AS-IV on hypoxia-induced oxidative stress and apoptosis in hippocampal neurons and explored its possible mechanism. In vivo, mice were placed in a hypoxic circulatory device containing 10% O2 and gavaged with AS-IV (60 and 120 mg/kg/d) for 4 weeks. In vitro, mouse hippocampal neuronal cells (HT22) were treated with hypoxia (1% O2) for 24 hours in the presence or absence of AS-IV, MDL-28170 (calpain-1 inhibitor), or YC-1 (HIF-1α inhibitor). The protective effect of AS-IV on brain injury was further explored by examining calpain-1 knockout mice. The results showed that hypoxia induced damage to hippocampal neurons, impaired spatial learning and memory abilities, and increased oxidative stress and apoptosis. Treatment with AS-IV or calpain-1 knockout improved the damage to hippocampal neurons and spatial learning and memory, attenuated oxidative stress and inhibited cell apoptosis. These changes were verified in HT22 cells. Overexpression of calpain-1 abolished the improvement of AS-IV on apoptosis and oxidative stress. In addition, the effects of AS-IV were accompanied by decreased calpain-1 and HIF-1α expression, and YC-1 showed a similar effect as AS-IV on calpain-1 and caspase-3 expression. In conclusion, this study demonstrates that AS-IV can downregulate the calpain-1/HIF-1α/caspase-3 pathway and inhibit oxidative stress and apoptosis of hippocampal neurons induced by hypoxia, which provides new ideas for studying the antiapoptotic activity of AS-IV.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"6509981"},"PeriodicalIF":3.0,"publicationDate":"2022-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10415175","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}

引用次数: 0

Low Intensity Noise Exposure Enhanced Auditory Loudness and Temporal Processing by Increasing Excitability of DCN. 低强度噪声暴露可通过提高直流神经网络的兴奋性来增强听觉响度和时序处理。

IF 3.1 4区医学

Neural Plasticity Pub Date : 2022-11-21 eCollection Date: 2022-01-01 DOI: 10.1155/2022/6463355

Lin Shi, Katie Palmer, Haolin Wang, Matthew A Xu-Friedman, Wei Sun

{"title":"Low Intensity Noise Exposure Enhanced Auditory Loudness and Temporal Processing by Increasing Excitability of DCN.","authors":"Lin Shi, Katie Palmer, Haolin Wang, Matthew A Xu-Friedman, Wei Sun","doi":"10.1155/2022/6463355","DOIUrl":"10.1155/2022/6463355","url":null,"abstract":"Sound stimulation is generally used for tinnitus and hyperacusis treatment. Recent studies found that long-term noise exposure can change synaptic and firing properties in the central auditory system, which will be detected by the acoustic startle reflex. However, the perceptual consequences of long-term low-intensity sound exposure are indistinct. This study will detect the effects of moderate-level noise exposure (83 dB SPL) on auditory loudness, and temporal processing was evaluated using CBA/CaJ mice. C-Fos staining was used to detect neural activity changes in the central auditory pathway. With two weeks of 83 dB SPL noise exposure (8 hours per day), no persistent threshold shift of the auditory brainstem response (ABR) was identified. On the other hand, noise exposure enhanced the acoustic startle response (ASR) and gap-induced prepulse inhibition significantly (gap-PPI). Low-level noise exposure, according to the findings, can alter temporal acuity. Noise exposure increased the number of c-Fos labeled neurons in the dorsal cochlear nucleus (DCN) and caudal pontine reticular nucleus (PnC) but not at a higher level in the central auditory nuclei. Our results suggested that noise stimulation can change acoustical temporal processing presumably by increasing the excitability of auditory brainstem neurons.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"6463355"},"PeriodicalIF":3.1,"publicationDate":"2022-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9705115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10772936","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}

引用次数: 0

Altered Effective Connectivity of the Primary Motor Cortex in Transient Ischemic Attack. 短暂性脑缺血发作时初级运动皮层有效连接性的改变

IF 3 4区医学

Neural Plasticity Pub Date : 2022-11-18 eCollection Date: 2022-01-01 DOI: 10.1155/2022/2219993

Zeqi Hao, Yulin Song, Yuyu Shi, Hongyu Xi, Hongqiang Zhang, Mengqi Zhao, Jiahao Yu, Lina Huang, Huayun Li

{"title":"Altered Effective Connectivity of the Primary Motor Cortex in Transient Ischemic Attack.","authors":"Zeqi Hao, Yulin Song, Yuyu Shi, Hongyu Xi, Hongqiang Zhang, Mengqi Zhao, Jiahao Yu, Lina Huang, Huayun Li","doi":"10.1155/2022/2219993","DOIUrl":"10.1155/2022/2219993","url":null,"abstract":"Objective: This study is aimed at exploring alteration in motor-related effective connectivity in individuals with transient ischemic attack (TIA).Methods: A total of 48 individuals with TIA and 41 age-matched and sex-matched healthy controls (HCs) were recruited for this study. The participants were scanned using MRI, and their clinical characteristics were collected. To investigate motor-related effective connectivity differences between individuals with TIA and HCs, the bilateral primary motor cortex (M1) was used as the regions of interest (ROIs) to perform a whole-brain Granger causality analysis (GCA). Furthermore, partial correlation was used to evaluate the relationship between GCA values and the clinical characteristics of individuals with TIA.Results: Compared with HCs, individuals with TIA demonstrated alterations in the effective connectivity between M1 and widely distributed brain regions involved in motor, visual, auditory, and sensory integration. In addition, GCA values were significantly correlated with high- and low-density lipoprotein cholesterols in individuals with TIA.Conclusion: This study provides important evidence for the alteration of motor-related effective connectivity in TIA, which reflects the abnormal information flow between different brain regions. This could help further elucidate the pathological mechanisms of motor impairment in individuals with TIA and provide a new perspective for future early diagnosis and intervention for TIA.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"2219993"},"PeriodicalIF":3.0,"publicationDate":"2022-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10790007","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}

引用次数: 0

Brain-Derived Neurotrophic Factor and Nerve Growth Factor Therapeutics for Brain Injury: The Current Translational Challenges in Preclinical and Clinical Research. 脑源性神经营养因子和神经生长因子治疗脑损伤：目前临床前和临床研究中的转化挑战。

IF 3 4区医学

Neural Plasticity Pub Date : 2022-03-02 eCollection Date: 2022-01-01 DOI: 10.1155/2022/3889300

Serena-Kaye Sims, Brynna Wilken-Resman, Crystal J Smith, Ashley Mitchell, Lilly McGonegal, Catrina Sims-Robinson

{"title":"Brain-Derived Neurotrophic Factor and Nerve Growth Factor Therapeutics for Brain Injury: The Current Translational Challenges in Preclinical and Clinical Research.","authors":"Serena-Kaye Sims, Brynna Wilken-Resman, Crystal J Smith, Ashley Mitchell, Lilly McGonegal, Catrina Sims-Robinson","doi":"10.1155/2022/3889300","DOIUrl":"10.1155/2022/3889300","url":null,"abstract":"Ischemic stroke and traumatic brain injury (TBI) are among the leading causes of death and disability worldwide with impairments ranging from mild to severe. Many therapies are aimed at improving functional and cognitive recovery by targeting neural repair but have encountered issues involving efficacy and drug delivery. As a result, therapeutic options for patients are sparse. Neurotrophic factors are one of the key mediators of neural plasticity and functional recovery. Neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) serve as potential therapeutic options to increase neural repair and recovery as they promote neuroprotection and regeneration. BDNF and NGF have demonstrated the ability to improve functional recovery in preclinical and to a lesser extent clinical studies. Direct and indirect methods to increase levels of neurotrophic factors in animal models have been successful in improving postinjury outcome measures. However, the translation of these studies into clinical trials has been limited. Preclinical experiments have largely failed to result in significant impacts in clinical research. This review will focus on the administration of these neurotrophic factors in preclinical and clinical stroke and TBI and the challenges in translating these therapies from the bench to the clinic.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"3889300"},"PeriodicalIF":3.0,"publicationDate":"2022-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8906958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10865392","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}

引用次数: 0

Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42. 降低电压门控钠通道β 2的表达可恢复Aβ1-42诱导的神经元损伤和改善认知功能障碍。

IF 3.1 4区医学

Neural Plasticity Pub Date : 2022-01-01 DOI: 10.1155/2022/3995227

Shan Li, Guo-Ji Yan, Ya-Xin Tan, Lu-Lu Xue, Ting-Hua Wang, Hao-Ran Zhao, Min-Nan Lu, Hui-Xiang Zhang, Rong Mei, Xiao-Han Dong, Li-Na Liu, Dan Wang, Yan-Bin Xiyang

{"title":"Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42.","authors":"Shan Li, Guo-Ji Yan, Ya-Xin Tan, Lu-Lu Xue, Ting-Hua Wang, Hao-Ran Zhao, Min-Nan Lu, Hui-Xiang Zhang, Rong Mei, Xiao-Han Dong, Li-Na Liu, Dan Wang, Yan-Bin Xiyang","doi":"10.1155/2022/3995227","DOIUrl":"https://doi.org/10.1155/2022/3995227","url":null,"abstract":"Voltage-gated sodium channel beta 2 (Nav2.2 or Navβ2, coded by SCN2B mRNA), a gene involved in maintaining normal physiological functions of the prefrontal cortex and hippocampus, might be associated with prefrontal cortex aging and memory decline. This study investigated the effects of Navβ2 in amyloid-β 1-42- (Aβ1-42-) induced neural injury model and the potential underlying molecular mechanism. The results showed that Navβ2 knockdown restored neuronal viability of Aβ1-42-induced injury in neurons; increased the contents of brain-derived neurotrophic factor (BDNF), enzyme neprilysin (NEP) protein, and NEP enzyme activity; and effectively altered the proportions of the amyloid precursor protein (APP) metabolites including Aβ42, sAPPα, and sAPPβ, thus ameliorating cognitive dysfunction. This may be achieved through regulating NEP transcription and APP metabolism, accelerating Aβ degradation, alleviating neuronal impairment, and regulating BDNF-related signal pathways to repair neuronal synaptic efficiency. This study provides novel evidence indicating that Navβ2 plays crucial roles in the repair of neuronal injury induced by Aβ1-42 both in vivo and in vitro.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"3995227"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9671742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10428829","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}

引用次数: 1

Ulinastatin Alleviates Repetitive Ketamine Exposure-Evoked Cognitive Impairment in Adolescent Mice. 乌司他丁减轻青春期小鼠重复氯胺酮暴露诱发的认知障碍。

IF 3.1 4区医学

Neural Plasticity Pub Date : 2022-01-01 DOI: 10.1155/2022/6168284

Yu Hong, Shiyu Meng, Shouping Wang, Ting Liu, Jiayi Liu

{"title":"Ulinastatin Alleviates Repetitive Ketamine Exposure-Evoked Cognitive Impairment in Adolescent Mice.","authors":"Yu Hong, Shiyu Meng, Shouping Wang, Ting Liu, Jiayi Liu","doi":"10.1155/2022/6168284","DOIUrl":"https://doi.org/10.1155/2022/6168284","url":null,"abstract":"Ketamine (KET) is widely used for induction and maintenance of anesthesia, and long-term use is required for treatment of depression patients. Repeated use of KET is associated with mood and memory disorders. Ulinastatin (UTI), a urinary trypsin inhibitor, has been widely undertaken as an anti-inflammatory drug and proved to have neuroprotective effects. The aim of this work was to determine whether prophylactic use of UTI could attenuate KET-induced cognitive impairment. It was found that repetitive KET anesthesia cause cognitive and emotional disorders in adolescent mice in WMZ and OFT test, while UTI pretreatment reversed the poor performance compared to the AK group, and the platform finding time and center crossing time were obviously short in the CK+UTI group (P < 0.05). Our ELISA experiment results discovered that UTI pretreatment reduced the expression levels of IL-1β and IL-6 induced by CK anesthesia compared to AK (P < 0.05). In addition, UTI pretreatment protected the cognitive function by restraining the expression levels of Tau protein, Tau phospho-396 protein, and Aβ protein in the CK group compared to the AK group in Western blotting (P < 0.05). The results suggested that UTI could act as a new strategy to prevent the neurotoxicity of KET, revealing a significant neuroprotective effect of UTI.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"6168284"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9763019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10772939","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}

引用次数: 1

Effect of TGF-β1-Mediated Exercise Analgesia in Spared Nerve Injury Mice. TGF-β1介导的运动镇痛对神经损伤小鼠的影响。

IF 3.1 4区医学

Neural Plasticity Pub Date : 2022-01-01 DOI: 10.1155/2022/7382327

Xinzheng Sun, Chenghao Wang, Junqi Wu, Xiaoke Chen, Hui He

{"title":"Effect of TGF-β1-Mediated Exercise Analgesia in Spared Nerve Injury Mice.","authors":"Xinzheng Sun, Chenghao Wang, Junqi Wu, Xiaoke Chen, Hui He","doi":"10.1155/2022/7382327","DOIUrl":"https://doi.org/10.1155/2022/7382327","url":null,"abstract":"Peripheral nerve injury leads to severe neuropathic pain. Previous studies have highlighted the beneficial effects of physical exercise on alleviating neuropathic pain. Exercise regulating transforming growth factor-β1 (TGF-β1) can improve several diseases and relieve neuropathic pain induced by peripheral nerve injury. Here, we investigated whether exercise could alleviate neuropathic pain by modulating TGF-β1 expression. We assessed mechanical and cold pain behavior and conducted molecular evaluation of the spinal cord. We found that spared nerve injury (SNI) led to mechanical and cold allodynia in the hind paw, elevated the expression of latency-associated peptide- (LAP-) TGF-β1, and activated astroglial in the spinal cord. Exercise decreases allodynia, astroglial activation, and LAP-TGF-β1 in SNI mice. Intrathecal injection of a TGF-type I receptor inhibitor attenuated exercise analgesia and enhanced astroglial activation. These findings demonstrate that exercise induces analgesia by promoting TGF-β1 activation and inhibiting astrogliosis. Our study reveals a new underlying mechanism for exercise-attenuated neuropathic pain in the maintenance stage of neuropathic pain after nerve injury.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"7382327"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9729053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10480023","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}

引用次数: 2

Protective Effects of Vitamin C against Neomycin-Induced Apoptosis in HEI-OC1 Auditory Cell. 维生素C对新霉素诱导HEI-OC1听觉细胞凋亡的保护作用

IF 3.1 4区医学

Neural Plasticity Pub Date : 2022-01-01 DOI: 10.1155/2022/1298692

Liang Gong, Biao Chen, Jingyuan Chen, Yongxin Li

{"title":"Protective Effects of Vitamin C against Neomycin-Induced Apoptosis in HEI-OC1 Auditory Cell.","authors":"Liang Gong, Biao Chen, Jingyuan Chen, Yongxin Li","doi":"10.1155/2022/1298692","DOIUrl":"https://doi.org/10.1155/2022/1298692","url":null,"abstract":"Ototoxic hearing loss results from hair cell death via reactive oxygen species (ROS) overproduction and consequent apoptosis. We investigated the effects of vitamin C (VC) on neomycin-induced HEI-OC1 cell damage, as well as the mechanism of inhibition. HEI-OC1 cells were treated with neomycin or with vitamin C (VC). The results indicated that VC had a protective effect on neomycin-induced HEI-OC1 cell death. Mechanistically, VC decreased neomycin-induced ROS generation, suppressed cell death, and increased cell viability. VC inhibited neomycin-induced apoptosis, ameliorated neomycin reduced antiapoptotic Bcl-2 expression, and suppressed neomycin increased expression of proapoptotic Bax, caspase-3 cleavage and caspase-8. TUNEL labeling demonstrated that VC blocked neomycin-induced apoptosis. Further study revealed that the effect of VC on neomycin-induced hair cell death was through interference with JNK activation and p38 phosphorylation. These results indicate that VC via suppressed ROS generation, which inhibited cell death by counteracting apoptotic signaling induced by neomycin in cells. Hence, VC is a potential candidate for protection agent against neomycin-induced HEI-OC1 cell ototoxicity.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"1298692"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9117069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10243311","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}

引用次数: 5

Predictive Power of Cognitive Biomarkers in Neurodegenerative Disease Drug Development: Utility of the P300 Event-Related Potential. 认知生物标志物在神经退行性疾病药物开发中的预测能力:P300事件相关电位的应用

IF 3.1 4区医学

Neural Plasticity Pub Date : 2022-01-01 DOI: 10.1155/2022/2104880

John Olichney, Jiangyi Xia, Kevin J Church, Hans J Moebius

{"title":"Predictive Power of Cognitive Biomarkers in Neurodegenerative Disease Drug Development: Utility of the P300 Event-Related Potential.","authors":"John Olichney, Jiangyi Xia, Kevin J Church, Hans J Moebius","doi":"10.1155/2022/2104880","DOIUrl":"https://doi.org/10.1155/2022/2104880","url":null,"abstract":"Neurodegenerative diseases, such as Alzheimer's disease (AD), and their associated deterioration of cognitive function are common causes of disability. The slowly developing pathology of neurodegenerative diseases necessitates early diagnosis and monitored long-term treatment. Lack of effective therapies coupled with an improved rate of early diagnosis in our aging population have created an urgent need for the development of novel drugs, as well as the need for reliable biomarkers for treatment response. These issues are especially relevant for AD, in which the rate of clinical trial drug failures has been very high. Frequently used biomarker evaluation procedures, such as positron emission tomography or cerebrospinal fluid measurements of phospho-tau and amyloid beta, are invasive and costly, and not universally available or accessible. This review considers the functionality of the event-related potential (ERP) P300 methodology as a surrogate biomarker for predicting the procognitive potential of drugs in clinical development for neurocognitive disorders. Through the application of standardized electroencephalography (EEG) described here, ERP P300 can be reliably measured. The P300 waveform objectively measures large-scale neuronal network functioning and working memory processes. Increased ERP P300 latency has been reported throughout the literature in disorders of cognition, supporting the potential utility of ERP P300 as a biomarker in many neurological and neuropsychiatric disorders, including AD. Specifically, evidence presented here supports ERP P300 latency as a quantitative, unbiased measure for detecting changes in cognition in patients with AD dementia through the progression from mild to moderate cognitive impairment and after drug treatment.","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2022 ","pages":"2104880"},"PeriodicalIF":3.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9666049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10483223","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}

引用次数: 4