Journal of experimental neurology最新文献

{"title":"Comparison of Different Post-Processing Algorithms for Dynamic Susceptibility Contrast Perfusion Imaging of Multiple Sclerosis Lesions: A Time to Peak Analysis","authors":"L. Monti, D. Momi, Tommaso Casseri, Davide Del Roscio, M. Bellini, Alessandro Rossi","doi":"10.33696/neurol.2.049","DOIUrl":"https://doi.org/10.33696/neurol.2.049","url":null,"abstract":"Objective: The purpose of the present study was to evaluate, in multiple sclerosis (MS) lesions, the diagnostic performance of two different commercial post-processing MR perfusion software. These two different algorithms for processing Dynamic susceptibility contrast (DSC) perfusion images have been used to differentiate perfusion values among white matter (WM) lesions, normal appearing white matter (NAWM), and grey matter (GM) in MS. The diagnostic performance for diff erentiating among lesions and normal tissue has been measured with respect to the Time to Peak (TTP). Methods and analysis: Analysing DSC perfusion imaging, a retrospective study has been performed on 74 MS patients and 15 normal subjects, by using 1.5 Tesla MRI scanner. TTP maps were generated by using 2 different commercially available algorithms (A;B). Analysis was conducted for the evaluation of diagnostic performance of different algorithms for differentiating between lesions and normal appearing WM and GM. Results: A statistically significant difference between the two algorithms was demonstrated by comparing TTP values among recent, stable lesions and NAWM. TTP values have been used to discriminate among recent, stable lesions and NAWM by using two different software packages. Conclusion: The optimal software should be that which increases the temporal resolution and be not operator dependent. TTP has been able to 1) examine the variability in the quantitative results of DSC MR perfusion imaging generated from identical source data of MS patients, 2) to identify the variables between two commercial post-processing algorithm and 3) to focus on the crucial role of post-processing inter-vendor differences.","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41528219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Commentary and Clinical Implications of “State of the Evidence Traffic Lights 2019: Systematic Review of Interventions for Preventing and Treating Children with Cerebral Palsy”","authors":"I. Novak, M. Paton, M. Finch-Edmondson, N. Badawi, Michael, Fahey, A. Velde, Ashleigh Hines, Leigha Dark, A. Khamis, Maria Mc Namara, E. Stanton, C. Morgan","doi":"10.33696/neurol.2.043","DOIUrl":"https://doi.org/10.33696/neurol.2.043","url":null,"abstract":"Iona Novak1,2*, Madison CB Paton2, Megan Finch-Edmondson2, Nadia Badawi2,3, Michael Fahey4,5, Annate Velde2, Ashleigh Hines2, Leigha Dark6, Amanda Khamis2, Maria Mc Namara2, Emma Stanton2, Cathy Morgan2 1Faculty of Medicine and Health, The University of Sydney, Sydney, Australia 2Cerebral Palsy Alliance Research Institute, Specialty of Child and Adolescent Health, Sydney Medical School, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45543496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Much is Known about Caregiver Burden in Dementia - What is Next? The Role of Comorb idities and Future Perspectives","authors":"G. Ransmayr, M. Defrancesco, A. Damulina, Philipp Hermann, Thomas, Benke, P. Dal-Bianco, J. Marksteiner, Alexandra Fuchs, F. Fellner, Andreas, Futschik, R. Schmidt","doi":"10.33696/neurol.2.042","DOIUrl":"https://doi.org/10.33696/neurol.2.042","url":null,"abstract":"Introduction and background: Care for family members suffering from neurological disorders is often demanding and increases with disease progression. Numerous patientand caregiver-related factors underlying caregiver burden have been identified. Some potential factors need to be clarified. Little is known about the effects of comorbidities and dementia complications on the burden of care for persons living with dementia. Objectives: We hypothesized that burdens of care for family members living with dementia increase with the number and severity of comorbidities and dementia complications. Methods: Multi-center prospective registry study (PRODEM) on caregiver burden in family caregivers (median age 61, 66% female) of 556 persons living with mild to moderate dementia, mainly Alzheimer’s disease (median age 77, 58% female). Results: Caregiver burden (Zarit Burden Interview) did not correlate with arterial hypertension, diabetes, hypercholesterolemia, cardioembolic/thromboembolic diagnoses, heart failure, severe arrhythmia or heart valve disease, but was worse in care recipients with symptoms of anxiety, psychotic episodes, depression and emotional, psychotic, behavioral and somatic symptom clusters (Neuropsychiatric Inventory, Geriatric Depression Scale-15 items). Moreover, caregiver burden correlated with the number of drugs taken daily. MRI evidence of cerebrovascular pathology (total volume of white matter hyperintensities on axial T2w-FLAIR sequences related to intracranial volume, measured in 301 patients) did not correlate with caregiver burden. Gerhard R, Defrancesco M, Damulina A, Hermann P, Benke T, Dal-Bianco P, et al. Much is Known about Caregiver Burden in Dementia What is Next? The Role of Comorbidities and Future Perspectives. J Exp Neurol. 2021;2(3):101-111. J Exp Neurol. 2021 Volume 2, Issue 3 102 Introduction and Background Care for patients with chronic debilitating neurological diseases is often demanding and can result in a variety of negative consequences including mental and physical morbidity. Numerous studies have been published on the burden of care for persons caring for spouses, parents, siblings or children with chronic neurological disorders, particularly for those who live with the care recipient and are directly responsible for care. Most studies address the care for dementia and stroke patients, persons with epilepsy, Parkinson’s disease and atypical parkinsonism, multiple sclerosis, motor neuron disease, Huntington’s disease, brain tumours, chronic pain syndromes, traumatic central nervous system injury, ataxias, and muscular dystrophy [1]. Little is known about caregiver burden in advanced stages of myasthenia gravis, adultonset myopathies, amyloidosis or other debilitating polyneuropathies or other rare neurological diseases. Most studies were performed in highor middle-income countries. The literature from low-income countries on family care for persons with chronic neurological diseases including dementia is spa","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46771352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Cellular Senescence on Neurodegenerative Diseases during the COVID-19 Pandemic: Sui table Targets Required to Eliminate Cellular Senescence","authors":"M. Mohiuddin, K. Kasahara","doi":"10.33696/neurol.2.046","DOIUrl":"https://doi.org/10.33696/neurol.2.046","url":null,"abstract":"We recently reviewed the scientific literature that elucidates the impact of cellular senescence on COVID-19 complications [1]. Recent studies have discussed the association of cellular senescence in COVID-19 patients with neurodegenerative diseases [2-5]. Therefore, in the present study, we extend this scientific synopsis to comment on how cellular senescence can promote neurodegenerative diseases and to describe suitable targets for eliminating cellular senescence.","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43169043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Spread of Spectrin in Ataxia and Neurodegenerative Disease","authors":"J. Morrow, Michael C. Stankewich","doi":"10.33696/neurol.2.045","DOIUrl":"https://doi.org/10.33696/neurol.2.045","url":null,"abstract":"Experimental and hereditary defects in the ubiquitous scaffolding proteins of the spectrin gene family cause an array of neuropathologies. Most recognized are ataxias caused by missense, deletions, or truncations in the SPTBN2 gene that encodes beta III spectrin. Such mutations disrupt the organization of post-synaptic receptors, their active transport through the secretory pathway, and the organization and dynamics of the actin-based neuronal skeleton. Similar mutations in SPTAN1 that encodes alpha II spectrin cause severe and usually lethal neurodevelopmental defects including one form of early infantile epileptic encephalopathy type 5 (West syndrome). Defects in these and other spectrins are implicated in degenerative and psychiatric conditions. In recent published work, we describe in mice a novel variant of alpha II spectrin that results in a progressive ataxia with widespread neurodegenerative change. The action of this variant is distinct, in that rather than disrupting a constitutive ligand-binding function of spectrin, the mutation alters its response to calcium and calmodulin-regulated signaling pathways including its response to calpain activation. As such, it represents a novel spectrinopathy that targets a key regulatory pathway where calcium and tyrosine kinase signals converge. Here we briefly discuss the various roles of spectrin in neuronal processes and calcium activated regulatory inputs that control its participation in neuronal growth, organization, and remodeling. We hypothesize that damage to the neuronal spectrin scaffold may be a common final pathway in many neurodegenerative disorders. Targeting the pathways that regulate spectrin function may thus offer novel avenues for therapeutic intervention.","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":"2 1","pages":"131 - 139"},"PeriodicalIF":0.0,"publicationDate":"2021-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48739559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural Population Computing: Parallel Distributed Processing, the Basal Ganglia, and Evolution","authors":"S. Nadeau","doi":"10.33696/neurol.2.038","DOIUrl":"https://doi.org/10.33696/neurol.2.038","url":null,"abstract":"It has been known for some time that representations in the central nervous system (CNS) are population encoded, that is, encoded as patterns of activity involving very large numbers of highly interconnected neurons in one or more neural networks extending over large expanses of the brain [1-11]. Nonetheless, understanding the computational processes occurring in pools of cortical neurons and the subcortical nuclei with which they interact continues to be one of the major challenges facing systems neuroscience.","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45821520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of B2-AR, TLR2, PICALM, and BDNF Gene Variants in Iranian Alzheimer’s Patients and Their Response to Rivastigmine","authors":"Parvin Mohabattalab, F. R. Rad, H. Zamani, Fariba Shirvani, M. Zamani","doi":"10.33696/neurol.2.041","DOIUrl":"https://doi.org/10.33696/neurol.2.041","url":null,"abstract":"Alzheimer’s disease (AD) is a devastating neurodegenerative disorder with polygenic and multifactorial inheritance, determined by progressive loss of memory and other cognitive functions. AD is characterized by hallmark pathological changes such as extracellular aggregation of amyloid β (Aβ), intraneuronal neurofibrillary tangles that lead to brain atrophy and loss of neural tissue [1,2]. Alzheimer’s disease is categorized according to the age of onset as early-onset (EOAD) or lateonset AD (LOAD) [3]. And, based on family history, it is classified as sporadic (SAD) or familial Alzheimer’s disease (FAD) [4]. There are various genetic and environmental factors involved in the pathogenesis of AD which makes the etiology of the disease complicated however, testing for Abstract","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42297986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Commentary on Vulnerability and Resilience to Activity-Based Anorexia and the Role of Dopamine.","authors":"Jeff A Beeler,&nbsp;Nesha S Burghardt","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Activity-based anorexia (ABA) is a commonly used rodent model of anorexia nervosa that is based on observations made in rats decades ago. In recently published work, we describe using this paradigm to model vulnerability and resilience to anorexia nervosa in mice, where vulnerability is characterized by hyperactivity and life-threatening weight loss and resilience is characterized by adaptation and weight stabilization. Using genetically modified hyperdopaminergic mice, we also demonstrate that increased dopamine augments vulnerability to ABA. Here, we briefly review our findings and discuss how obtaining vulnerable and resilient phenotypes enhances utility of the ABA model for understanding the neurobiological basis of anorexia nervosa. We comment on our dopamine findings and close by discussing implications for clinical treatment.</p>","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":" ","pages":"21-28"},"PeriodicalIF":0.0,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7990270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25517672","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":"Commentary: Use of BACTRAC Proteomic Database-Uromodulin Protein Expression During Ischemic Stroke.","authors":"Gabriella-Salome K Armstrong,&nbsp;Jacqueline A Frank,&nbsp;Christopher J McLouth,&nbsp;Ann Stowe,&nbsp;Jill M Roberts,&nbsp;Amanda L Trout,&nbsp;Justin F Fraser,&nbsp;Keith Pennypacker","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Uromodulin (UMOD) is a glycoprotein expressed by the epithelial cells of the thick ascending limb of Henle's loop in the kidney. Research has shown that increased uromodulin expression may be associated with lower risk of cardiovascular disease in adults. Utilizing the Blood and Clot Thrombectomy Registry and Collaboration (BACTRAC) (clinicaltrials.gov NCT03153683), a continuously enrolling tissue bank, we aimed to examine the associations between serum uromodulin, age, and high BMI (BMI>25) and its relationship to stroke in patients.</p><p><strong>Methods: </strong>Arterial blood distal and proximal to the thrombus was collected during a thrombectomy procedure using the BACTRAC protocol and sent to Olink (Boston, MA) to determine proteomic expression via proximity extension assay. Uromodulin expression was recorded and analyzed using two tailed T-tests and linear regressions.</p><p><strong>Results: </strong>The relationship between systemic and intracranial uromodulin, age, high BMI and hypertension were assessed. Systemic and intracranial uromodulin decreased with age (p<0.0001 and r²=0.343, p=0.0416 and r²=0.102) respectively. Systemic uromodulin expression increased with BMI>25 (p=0.014). Presence of hypertension decreased uromodulin's expression systemically (p=0.018) and intracranially (p=0.007).</p><p><strong>Conclusions: </strong>Uromodulin was increased significantly in overweight patients, decreased significantly in older patients, and decreased in patients with hypertension. The increase in uromodulin in people with high BMI could be a protective reaction of the kidney to worsening conditions that make ischemic stroke more likely, with a goal of delaying dangerous outcomes. The decreased expression of uromodulin in older adults could be associated with the decline of general kidney function that accompanies aging. Hypertension can contribute to an AKI by decreasing perfusion to the kidney, therefore decreasing kidney function and uromodulin production. Further analyses are needed to understand the role of uromodulin following ischemic stroke.</p>","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":"2 1","pages":"29-33"},"PeriodicalIF":0.0,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7990290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9246699","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":"Commentary: Use of BACTRAC Proteomic Database-Uromodulin Protein Expression During Ischemic Stroke","authors":"Gabriella-Salome K. Armstrong, J. Frank, C. McLouth, A. Stowe, Jill M Roberts, A. Trout, J. Fraser, K. Pennypacker","doi":"10.33696/NEUROL.2.032","DOIUrl":"https://doi.org/10.33696/NEUROL.2.032","url":null,"abstract":"Introduction: Uromodulin (UMOD) is a glycoprotein expressed by the epithelial cells of the thick ascending limb of Henle’s loop in the kidney. Research has shown that increased uromodulin expression may be associated with lower risk of cardiovascular disease in adults. Utilizing the Blood and Clot Thrombectomy Registry and Collaboration (BACTRAC) (clinicaltrials.gov NCT03153683), a continuously enrolling tissue bank, we aimed to examine the associations between serum uromodulin, age, and high BMI (BMI>25) and its relationship to stroke in patients. Methods: Arterial blood distal and proximal to the thrombus was collected during a thrombectomy procedure using the BACTRAC protocol and sent to Olink (Boston, MA) to determine proteomic expression via proximity extension assay. Uromodulin expression was recorded and analyzed using two tailed T-tests and linear regressions. Results: The relationship between systemic and intracranial uromodulin, age, high BMI and hypertension were assessed. Systemic and intracranial uromodulin decreased with age (p<0.0001 and r2=0.343, p=0.0416 and r2=0.102) respectively. Systemic uromodulin expression increased with BMI>25 (p=0.014). Presence of hypertension decreased uromodulin’s expression systemically (p=0.018) and intracranially (p=0.007). Conclusions: Uromodulin was increased significantly in overweight patients, decreased significantly in older patients, and decreased in patients with hypertension. The increase in uromodulin in people with high BMI could be a protective reaction of the kidney to worsening conditions that make ischemic stroke more likely, with a goal of delaying dangerous outcomes. The decreased expression of uromodulin in older adults could be associated with the decline of general kidney function that accompanies aging. Hypertension can contribute to an AKI by decreasing perfusion to the kidney, therefore decreasing kidney function and uromodulin production. Further analyses are needed to understand the role of uromodulin following ischemic stroke.","PeriodicalId":73744,"journal":{"name":"Journal of experimental neurology","volume":"2 1","pages":"29 - 33"},"PeriodicalIF":0.0,"publicationDate":"2021-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43263330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}