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| 1 | Anionic liposomes for small interfering ribonucleic acid (siRNA) delivery to primary neuronal cells: Evaluation of alpha-synuclein knockdown efficacy显示文摘Alpha-synuclein (在 Lewy 身体(磅) 的 -syn) 免职是 Parkinsons 疾病(PD ) 的主要 neuropathological 特点之一。磅累积被认为 PD 的一个原因的因素,它建议针对减少 -syn 层次的策略能为它的处理是相关的。在现在的学习,我们开发了对明确地被设计由 RNA 干扰减少 neuronal -syn 的小介入核糖核酸酸(siRNA ) 的全身的交货合适的新奇 nanocarriers。当一个指向的代理人被准备,与为 -syn 基因 silencing 复杂、与狂犬病病毒 glycoprotein (RVG ) 装饰的 siRNA 鱼精朊装载的 Anionic liposomes 导出肽。nanoparticles 为他们装载,保护,并且交付到老鼠的功能的 siRNA 的能力被描绘象他们的效率到一样的主要海马趾、外皮的神经原在这些房间导致基因 silencing。而且, nanocarriers 在浆液为他们的稳定性被评估。装饰 RVG 的 liposomes 在 vivo 应用程序为未来显示了合适的特征并且没有改变房间生存能力,成功地在主要神经原导致了 -syn 基因 silencing。一起,我们的结果显示装饰 RVG 的 liposomes 可以是为针对完成的进一步的研究的一个理想的工具在在 PD 的老鼠模型的 vivo -syn 基因 silencing 有效。 | Michele Schlich Francesca Longhena Gaia Faustini Caitriona M. O'Driscoll Chiara Sinico Anna Maria Fadda Arianna Bellucci Francesco Lai | 2017 | Nano Research2017，10，10： | 1 |
| 2 | Mitochondrial Dysfunction and alpha-Synuelein Synaptic Pathology in Parkinson's Disease: Who's on First?显示文摘 | Zaltieri M Longhena F Pizzi M | 2015 | Parkinson''s disease2015，2015，10： | 1 |
| 3 | Mitochondrial Dysfunction and α -Synuclein Synaptic Pathology in Parkinson’s Disease: Who’s on First?显示文摘 | Michela Zaltieri Francesca Longhena Marina Pizzi Cristina Missale PierFranco Spano Arianna Bellucci Patrick Lewis | 2015 | Parkinson’s Disease2015，，： | 1 |
| 4 | NF-κB/c-Rel deficiency causes Parkinson’s disease-like prodromal symptoms and progressive pathology in mice显示文摘Background:Parkinson’s disease(PD),the most common neurodegenerative movement disorder,is characterized by dopaminergic nigrostriatal neuron loss and brain accumulation of Lewy bodies,protein aggregates mainly composed ofα-synuclein.We reported that mice deficient for NF-κB/c-Rel(c-rel^(-/-))develop a late-onset parkinsonism.At 18 months of age,c-rel^(-/-)mice showed nigrostriatal degeneration and accumulation ofα-synuclein aggregates associated with a motor impairment responsive to L-DOPA administration.Being c-Rel protein a transcriptional regulator for mitochondrial anti-oxidant and antiapoptotic factors,it has been inferred that its deficiency may affect the resilience of“energy demanding”nigral dopaminergic neurons to the aging process.PD patients manifest a prodromal syndrome that includes olfactory and gastrointestinal dysfunctions years before the frank degeneration of nigrostriatal neurons and appearance of motor symptoms.According to the Braak staging,the onset of non-motor and motor symptoms relates to progressive ascendant diffusion ofα-synuclein pathology in the brain.The aim of this study was to identify whether c-rel^(-/-)deficiency is associated with the onset of premotor signs of PD and spatio-temporal progression of cerebralα-synuclein deposition.Methods:Intestinal and olfactory functions,intestine and brainα-synuclein deposition as well as striatal alterations,were assessed in c-rel^(-/-)and control mice from 2 to 18 months of age.Results:From 2 months of age,c-rel^(-/-)mice displayed intestinal constipation and increasing olfactory impairment.At 2 months,c-rel^(-/-)mice exhibited a mildα-synuclein accumulation in the distal colon.Moreover,they developed an agedependent deposition of fibrillaryα-synuclein that,starting at 5 months from the olfactory bulbs,dorsal motor nucleus of vagus and locus coeruleus,reached the substantia nigra at 12 months.At this age,theα-synuclein pathology associated with a drop of dopamine transporter in the striatum that anticipated by 6 months the axonal degeneration.From 12 months onwards oxidative/nitrosative stress developed in the striatum in parallel with altered expression of mitochondrial homeostasis regulators in the substantia nigra.Conclusions:In c-rel^(-/-)mice,reproducing a parkinsonian progressive pathology with non-motor and motor symptoms,a Braak-like pattern of brain ascendingα-synuclein deposition occurs.The peculiar phenotype of c-rel^(-/-)mice envisages a potential contribution of c-Rel dysregulation to the pathogenesis of PD. | Edoardo Parrella Arianna Bellucci Vanessa Porrini Marina Benarese Annamaria Lanzillotta Gaia Faustini Francesca Longhena Giulia Abate Daniela Uberti Marina Pizzi | 2019 | Translational Neurodegeneration2019，8，1： | 1 |
| 5 | Study of alpha-synuclein fibrillation: state of the art and expectations显示文摘Since the discovery of the presence of fibrillary forms ofα-synuclein(α-syn)in Lewy bodies(LB)and Lewy neurites in the brain of patients affected by Parkinson’s disease(PD)and dementia with LB,great effort has been dedicated to study the features ofα-syn fibrillation.In parallel,the pathological relevance of the different toxic forms ofα-syn has been also matter of investigation.In the last twenty years,scientists have been able to single out thatα-syn fibrillation initiates pathological mechanisms that by contributing to or triggering neurodegeneration/neuroinflammation,may lead to PD pathogenesis.This notwithstanding,we still ignore the reasons whyα-syn shifts from its natively unfolded conformation to toxic oligomeric and fibrillary forms.The chameleonic nature of monomericα-syn,and the extremely polymorphic characteristics of aggregated strains,renders it difficult to picture the real nature ofα-syn fibrils,their exact composition and formation dynamics.Recently,sophisticated biophysical methods and microscopy techniques have been exploited to studyα-syn fibrillation.Here,we provide an overview of the most relevant advancement in our understanding ofα-syn fibrils formation and conformation. | Francesca Longhena Gaia Faustini Arianna Bellucci | 2020 | Neural Regeneration Research2020，15，1： | 0 |
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