Neurodegenerative Diseases最新文献

{"title":"Postoperative Cognitive Dysfunction and the Protective Effects of Enriched Environment: A Systematic Review.","authors":"Momin Hua,&nbsp;Jia Min","doi":"10.1159/000513196","DOIUrl":"https://doi.org/10.1159/000513196","url":null,"abstract":"<p><strong>Background: </strong>Currently, the number of individuals who undergo surgery is greatly increased. As a consequence, postoperative cognitive dysfunction (POCD) has gradually gained more attention.</p><p><strong>Summary: </strong>POCD is a perioperative complication requiring sensitive preoperative and postoperative neuropsychiatric tests, and its incidence in both cardiac and noncardiac surgery is high, especially in elderly individuals. Surgical, patient, and anesthetic factors may all lead to the occurrence and development of POCD. The key mechanism of POCD may be the inflammatory response of the central nervous system during surgery, which is similar to that of Alzheimer's disease (AD). Enriched environment (EE), a factor that can significantly improve and prevent neurodegenerative diseases, may have a beneficial effect on POCD. Key Messages: This review aims to elucidate the mechanism of the occurrence and development of POCD, analyze the possible influence of EE on POCD at the molecular level, and provide a direction for its treatment.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"20 4","pages":"113-122"},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000513196","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25380848","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}

{"title":"Diffusion Tensor Imaging Reveals Whole-Brain Microstructural Changes in the P301L Mouse Model of Tauopathy.","authors":"Aidana Massalimova,&nbsp;Ruiqing Ni,&nbsp;Roger M Nitsch,&nbsp;Marco Reisert,&nbsp;Dominik von Elverfeldt,&nbsp;Jan Klohs","doi":"10.1159/000515754","DOIUrl":"https://doi.org/10.1159/000515754","url":null,"abstract":"<p><strong>Introduction: </strong>Increased expression of hyperphosphorylated tau and the formation of neurofibrillary tangles are associated with neuronal loss and white matter damage. Using high-resolution ex vivo diffusion tensor imaging (DTI), we investigated microstructural changes in the white and grey matter in the P301L mouse model of human tauopathy at 8.5 months of age. For unbiased computational analysis, we implemented a pipeline for voxel-based analysis (VBA) and atlas-based analysis (ABA) of DTI mouse brain data.</p><p><strong>Methods: </strong>Hemizygous and homozygous transgenic P301L mice and non-transgenic littermates were used. DTI data were acquired for generation of fractional anisotropy (FA), mean diffusivity (MD), radial diffusivity (RD), and axial diffusivity (AD) maps. VBA on the entire brain was performed using SPM8 and the SPM Mouse toolbox. Initially, all DTI maps were coregistered with the Allen mouse brain atlas to bring them to one common coordinate space. In VBA, coregistered DTI maps were normalized and smoothed in order to perform two-sample and unpaired t tests with false discovery rate correction to compare hemizygotes with non-transgenic littermates, homozygotes with non-transgenic littermates, and hemizygotes with homozygotes on each DTI parameter map. In ABA, the average values for selected regions of interests were computed with coregistered DTI maps and labels in Allen mouse brain atlas. Afterwards, a Kruskal-Wallis one-way ANOVA on ranks with a Tukey post hoc test was executed on the estimated average values.</p><p><strong>Results: </strong>With VBA, we found pronounced and brain-wide spread changes when comparing homozygous, P301L mice with non-transgenic littermates, which were not seen when comparing hemizygous P301L with non-transgenic animals. Statistical comparison of DTI metrics in selected brain regions by ABA corroborated findings from VBA. FA was found to be decreased in most brain regions, while MD, RD, and AD were increased in homozygotes compared to hemizygotes and non-transgenic littermates.</p><p><strong>Discussion/conclusion: </strong>High-resolution ex vivo DTI demonstrated brain-wide microstructural and gene-dose-dependent changes in the P301L mouse model of human tauopathy. The DTI analysis pipeline may serve for the phenotyping of models of tauopathy and other brain diseases.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"20 5-6","pages":"173-184"},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000515754","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38901345","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}

{"title":"The Effects of 8-Week Combined Exercise Training on Inflammatory Markers in Women with Multiple Sclerosis.","authors":"Fahime Tadayon Zadeh,&nbsp;Hamid Amini,&nbsp;Saeed Habibi,&nbsp;Valiallah Shahedi,&nbsp;Amin Isanejad,&nbsp;Mohsen Akbarpour","doi":"10.1159/000518580","DOIUrl":"https://doi.org/10.1159/000518580","url":null,"abstract":"<p><strong>Purpose: </strong>The present study was designed to investigate the effects of 8-week combined endurance, resistance, and balance exercise training on IL-6, CRP, and IL-10 concentrations in women with multiple sclerosis.</p><p><strong>Methods: </strong>Thirty participants with multiple sclerosis (Expanded Disability Status Scale ≤6) were randomized into either an exercise and control groups. The exercise group performed 8-weeks of endurance, resistance, and balance exercise training. Serum concentrations of IL-6, CRP, and IL-10 were measured before and after the 8-week intervention. Moreover, anthropometric measures were determined at the onset of and after the intervention. For within- and between groups comparisons of all variables, t test (independent and dependent) was used (p < 0.05).</p><p><strong>Results: </strong>The results revealed that IL-6 and CRP levels significantly decreased after exercise training (from 6.8 ± 1.52 to 3.2 ± 0.96, p < 0.001 and from 2.76 ± 0.98 to 1.55 ± 0.44, p = <0.001; respectively). Also, exercise training significantly increased IL-10 in the exercise group (from 16.4 ± 2.74 to 23.2 ± 2.11, p < 0.001). There was a significant difference between the 2 groups in all markers in the after 8-week exercise (p < 0.05).</p><p><strong>Conclusions: </strong>One of the characteristics of MS disease is inflammation. Exercise training through physiological mechanisms and without aggravating the inflammatory pathology can be effective in functional and symptom reduction of patients with MS. In confirmation of this, the present study showed that 8 weeks of combined exercise training decreased pro-inflammatory markers (IL-6 and CRP) and increased anti-inflammatory cytokine (IL-10). Our findings suggested that an exercise training program can be an effective strategy for managing the immune system of women with MS at least by its significant effect on inflammatory markers.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"20 5-6","pages":"212-216"},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000518580","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39274498","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}

{"title":"Contents Vol. 20, 2020","authors":"","doi":"10.1159/000519819","DOIUrl":"https://doi.org/10.1159/000519819","url":null,"abstract":"","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"1 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65298483","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}

{"title":"Elevated Levels of Homocysteinesulfinic Acid in the Plasma of Patients with Amyotrophic Lateral Sclerosis: A Potential Source of Excitotoxicity?","authors":"Aven Lee,&nbsp;Buddhika Jayakody Arachchige,&nbsp;Robert Henderson,&nbsp;James Aylward,&nbsp;Pamela Ann McCombe","doi":"10.1159/000517964","DOIUrl":"https://doi.org/10.1159/000517964","url":null,"abstract":"<p><strong>Objectives: </strong>Excitotoxicity is thought to be involved in the pathogenesis of amyotrophic lateral sclerosis (ALS). One possible source of excitotoxicity is the presence of sulphur amino acids (SAAs). In the brain of subjects with ALS, there are increased levels of taurine. In the metabolism of methionine to taurine, excitatory sulphur amino acids (SAAs) are formed. These could potentially contribute to excitotoxicity in ALS. The present study has examined whether plasma levels of SAAs in 38 ALS patients differ from those of 30 healthy controls.</p><p><strong>Methods: </strong>Plasma levels of SAAs were measured by liquid chromatography mass spectrometry.</p><p><strong>Results: </strong>There were no significant changes in plasma cysteic acid, cysteine sulfinic acid, and homocysteic acid in ALS patients compared to healthy subjects. Significant elevations in plasma homocysteinesulfinic acid (HCSA) levels (p < 0.0001) were observed in the ALS patients (75.91 ± 15.38 nM) compared to healthy controls (54.06 ± 8.503 nM); 50% of the ALS patients had HCSA levels that were 1.5-2-folds higher than those of controls. Plasma levels of HCSA differed significantly (p = 0.0440) between patients with bulbar onset and spinal onset (68.57 ± 14.20 vs. 79.30 ± 14.95 nM, respectively).</p><p><strong>Conclusion: </strong>HCSA is elevated in the blood of subjects with ALS. Since HCSA can be transported from the blood to the CNS by active transport, has neurotransmitter properties, and can activate synaptic receptors including NMDAR and metabotropic glutamate receptor, it is possible that increases in HCSA could influence glutamatergic neurotransmission and potentially contribute to excitotoxicity in some ALS patients.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"20 5-6","pages":"200-206"},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000517964","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39275602","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}

{"title":"Extending the Spectrum of Nonmotor Symptoms with Olfaction in Premotor Huntington's Disease: A Pilot Study.","authors":"Beatrice Heim,&nbsp;Dora Valent,&nbsp;Federico Carbone,&nbsp;Sabine Spielberger,&nbsp;Florian Krismer,&nbsp;Atbin Djamshidian-Tehrani,&nbsp;Klaus Seppi","doi":"10.1159/000518136","DOIUrl":"https://doi.org/10.1159/000518136","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this pilot study was to investigate change of olfactory functions in Huntington's disease (HD).</p><p><strong>Background: </strong>HD is a neurodegenerative disease characterized by motor, cognitive, and behavioral abnormalities. There are several studies reporting olfactory dysfunction in manifest and some studies in premanifest HD carriers, and a recent neuropathological study demonstrated HD-specific protein aggregation in the anterior olfactory nucleus in HD patients. In this study, we wanted to assess olfactory functions as a possible early nonmotor symptom of HD mutation carriers without disease-specific motor symptoms and HD patients.</p><p><strong>Methods: </strong>All participants had genetic confirmed HD and were prospectively recruited during their routine control in a specialized outpatient clinic of the Medical University of Innsbruck, Department of Neurology, Austria. Healthy controls (HCs) were caregivers from patients. They were only included if they were younger than 70 years, scored more than 24/30 points on the Mini Mental State Examination, and had no other disease compromising olfactory function. Furthermore, all participants were tested on the Sniffin' sticks 16-items identification test.</p><p><strong>Results: </strong>We included 23 patients with manifest HD, 13 HD mutation carriers, and 19 HCs. Mutation carriers showed significant impaired odor identification compared to HCs (p < 0.001), as well as Huntington's patients compared with both mutation carriers (p = 0.003) and HCs (p < 0.001).</p><p><strong>Conclusions: </strong>The results of this pilot study suggest that olfactory dysfunction may be an early nonmotor symptom of HD and could be a potential marker to assess disease progression.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"20 5-6","pages":"207-211"},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000518136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39275192","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}

{"title":"Alpha-Synuclein: The Interplay of Pathology, Neuroinflammation, and Environmental Factors in Parkinson's Disease.","authors":"Songzhe He,&nbsp;Shan Zhong,&nbsp;Gang Liu,&nbsp;Jun Yang","doi":"10.1159/000511083","DOIUrl":"https://doi.org/10.1159/000511083","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease (PD) is a multifactorial, chronic, and progressive neurodegenerative disease. α-Synuclein (α-syn), which is the main protein component of Lewy bodies, plays an important role in the pathological hallmarks of PD. However, the pathological function of α-syn and the molecular mechanisms responsible for the degeneration of dopaminergic neurons are still elusive.</p><p><strong>Summary: </strong>Cumulative evidence implicates that abnormal processing of α-syn will be predicted to lead to pathological changes in PD. Key Messages: In this review, we summarize the structure and physiological function of α-syn, and further discuss the interplay of pathology, neuroinflammation, and environmental factors in PD. Additionally, we suggest future directions for understanding the toxicity of α-syn to neurons, which may ultimately encourage us to better design disease-modifying therapeutic strategies for PD.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"20 2-3","pages":"55-64"},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000511083","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38835181","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}

{"title":"Ferroptosis Is Regulated by Mitochondria in Neurodegenerative Diseases.","authors":"Juepu Zhou,&nbsp;Yao Jin,&nbsp;Yuhong Lei,&nbsp;Tianyi Liu,&nbsp;Zheng Wan,&nbsp;Hao Meng,&nbsp;Honglei Wang","doi":"10.1159/000510083","DOIUrl":"https://doi.org/10.1159/000510083","url":null,"abstract":"<p><strong>Background: </strong>Neurodegenerative diseases are characterized by a gradual decline in motor and/or cognitive function caused by the selective degeneration and loss of neurons in the central nervous system, but their pathological mechanism is still unclear. Previous research has revealed that many forms of cell death, such as apoptosis and necrosis, occur in neurodegenerative diseases. Research in recent years has noticed that there is a new type of cell death in neurodegenerative diseases: ferroptosis. An increasing body of literature provides evidence for an involvement of ferroptosis in neurodegenerative diseases.</p><p><strong>Summary: </strong>In this article, we review a new form of cell death in neurodegenerative diseases: ferroptosis. Ferroptosis is defined as an iron-dependent form of regulated cell death, which occurs through the lethal accumulation of lipid-based reactive oxygen species when glutathione-dependent lipid peroxide repair systems are compromised. Several salient and established features of neurodegenerative diseases (including lipid peroxidation and iron dyshomeostasis) are consistent with ferroptosis, which means that ferroptosis may be involved in the progression of neurodegenerative diseases. In addition, as the center of energy metabolism in cells, mitochondria are also closely related to the regulation of iron homeostasis in the nervous system. At the same time, neurodegenerative diseases are often accompanied by degeneration of mitochondrial activity. Mitochondrial damage has been found to be involved in lipid peroxidation and iron dyshomeostasis in neurodegenerative diseases. Key Messages: Based on the summary of the related mechanisms of ferroptosis, we conclude that mitochondrial damage may affect neurodegenerative diseases by regulating many aspects of ferroptosis, including cell metabolism, iron dyshomeostasis, and lipid peroxidation.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"20 1","pages":"20-34"},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000510083","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38278668","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}

{"title":"Cerebrospinal Fluid Alzheimer's Biomarkers and Neurofilament Light Profile of Idiopathic Normal Pressure Hydrocephalus in China: A PUMCH Cohort Study.","authors":"Chenhui Mao,&nbsp;Longze Sha,&nbsp;Caiyan Liu,&nbsp;Shanshan Chu,&nbsp;Jie Li,&nbsp;Xinying Huang,&nbsp;Dan Lei,&nbsp;Jie Wang,&nbsp;Liling Dong,&nbsp;Qi Xu,&nbsp;Bin Peng,&nbsp;Li-Ying Cui,&nbsp;Jing Gao","doi":"10.1159/000514052","DOIUrl":"https://doi.org/10.1159/000514052","url":null,"abstract":"<p><strong>Introduction: </strong>Idiopathic normal pressure hydrocephalus (iNPH) is one of the potentially reversible dementias. Early and accurate diagnosis is important for patients' prognosis. Emerging evidence shows fluid biomarkers are useful in diagnosis and pathophysiological research of iNPH.</p><p><strong>Methods: </strong>Probable iNPH and Alzheimer's disease (AD) patients were recruited. Clinical diagnosis was performed according to international guidelines. CSF collection complied with a standard protocol. Commercial accessible ELISA kits were introduced for measurement of CSF t-tau, p-tau181, Aβ42, and NfL.</p><p><strong>Results: </strong>Twenty-seven iNPH, 27 AD, and 18 controls were included. The profiles of CSF t-tau, p-tau181, and t-tau/Aβ42 in the iNPH and AD were significantly different (p < 0.0001). The profiles of CSF t-tau, p-tau181, and t-tau/Aβ42 in the iNPH and control were not different (p > 0.05). Level of CSF Aβ42 in iNPH was significantly lower than control (p < 0.0001) and also significantly higher than AD (p < 0.05). NfL level in iNPH and AD was increased, but its level in iNPH was significantly lower than that in AD (p = 0.005). NfL and t-tau level in the iNPH group was significantly correlated (coefficient = 0.649, p = 0.005), but not in AD (coefficient = 0.298, p = 0.157).</p><p><strong>Conclusion: </strong>Alzheimer's CSF biomarker profile of iNPH subjects showed moderately decreased Aβ42 and normal t-tau, p-tau181, and t-tau/Aβ42, which was distinguishable from AD. The different profiles and correlation of t-tau and NfL suggested different pathophysiology of AD and iNPH. t-tau was relatively an AD-specific neurodegenerative biomarker compared to NfL.</p>","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"20 5-6","pages":"165-172"},"PeriodicalIF":3.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000514052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39054291","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}

{"title":"Assessment of the Corticospinal Tract Profile in Pure Lower Motor Neuron Disease: A Diffusion Tensor Imaging Study","authors":"A. Sarica, P. Valentino, R. Nisticó, S. Barone, F. Pucci, A. Quattrone, A. Cerasa, A. Quattrone","doi":"10.1159/000503970","DOIUrl":"https://doi.org/10.1159/000503970","url":null,"abstract":"Aim: The aim of this study was to evaluate the corticospinal tract (CST) diffusion profile in pure lower motor neuron disease (pLMND) patients who at baseline did not show any clinical or electrophysiological involvement of upper motor neurons (UMN), and in amyotrophic lateral sclerosis (ALS) patients. Materials and Methods: Fifteen ALS patients with delayed central motor conduction time (CMCT) and 14 pLMND patients with normal CMCT were enrolled together with 15 healthy controls. Fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD) maps were obtained. The tract profile of CST was reconstructed with the automated fiber quantification tool and its diffusion properties were quantified voxel-by-voxel and then compared pairwise between groups. Moreover, a random forest (RF) classifier was trained to evaluate the ability of CST diffusion metrics in distinguishing pairwise the groups from the controls. Results: ALS patients presented wide microstructural abnormalities in the entire CST as assessed by FA decrease and RD increase while pLMND patients showed focal FA decrease and a larger AD increase in the cerebral peduncle and posterior limb of the internal capsule in comparison with controls. RF revealed that diffusion tensor imaging (DTI) metrics accurately distinguished ALS patients and pLMND patients from controls (96.67 and 95.71% accuracy, respectively). Conclusions: Our study demonstrates that the CST was impaired in both ALS and pLMND patients, thus suggesting that DTI metrics are a reliable tool in detecting subtle changes of UMN in pLMND patients, also in the absence of clinical and CMCT abnormalities.","PeriodicalId":19115,"journal":{"name":"Neurodegenerative Diseases","volume":"19 1","pages":"128 - 138"},"PeriodicalIF":3.0,"publicationDate":"2019-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000503970","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49660526","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}