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| 1 | The potential of bone morphogenetic protein 2 as a neurotrophic factor for Parkinson’s disease显示文摘Parkinson’s disease is the second most common neurodegenerative disorder;it affects 1%of the population over the age of 65.The number of people with Parkinson’s disease is set to rapidly increase due to changing demographics and there is an unmet clinical need for disease-modifying therapies.The pathological hallmarks of Parkinson’s disease are the progressive degeneration of dopaminergic neurons in the substantia nigra and their axons which project to the striatum,and the aggregation ofα-synuclein;these result in a range of debilitating motor and non-motor symptoms.The application of neurotrophic factors to protect and potentially regenerate the remaining dopaminergic neurons is a major area of research interest.However,this strategy has had limited success to date.Clinical trials of two well-known neurotrophic factors,glial cell line-derived neurotrophic factor and neurturin,have reported limited efficacy in Parkinson’s disease patients,despite these factors showing potent neurotrophic actions in animal studies.There is therefore a need to identify other neurotrophic factors that can protect againstα-synuclein-induced degeneration of dopaminergic neurons.The bone morphogenetic protein(BMP)family is the largest subgroup of the transforming growth factor-βsuperfamily of proteins.BMPs are naturally secreted proteins that play crucial roles throughout the developing nervous system.Importantly,many BMPs have been shown to be potent neurotrophic factors for dopaminergic neurons.Here we discuss recent work showing that transcripts for the BMP receptors and BMP2 are co-expressed with several key markers of dopaminergic neurons in the human substantia nigra,and evidence for downregulation of BMP2 expression at distinct stages of Parkinson’s disease.We also discuss studies that explored the effects of BMP2 treatment,in in vitro and in vivo models of Parkinson’s disease.These studies found potent effects of BMP2 on dopaminergic neurites,which is important given that axon degeneration is increasingly recognized as a key early event in Parkinson’s disease.Thus,the aim of this mini-review is to give an overview of the BMP family and the BMP-Smad signalling pathway,in addition to reviewing the available evidence demonstrating the potential of BMP2 for Parkinson’s disease therapy. | Susan R.Goulding Aideen M.Sullivan Gerard W.O’Keeffe Louise M.Collins | 2020 | Neural Regeneration Research2020，15，8： | 7 |
| 2 | Neurotrophic factors: from neurodevelopmental regulators to novel therapies for Parkinson's disease显示文摘Neuroprotection and neuroregeneration are two of the most promising disease-modifying therapies for the incurable and widespread Parkinson's disease. In Parkinson's disease, progressive degeneration of nigrostriatal dopaminergic neurons causes debilitating motor symptoms. Neurotrophic factors play important regulatory roles in the development, survival and maintenance of specific neuronal populations. These factors have the potential to slow down, halt or reverse the loss of nigrostriatal dopaminergic neurons in Parkinson's disease. Several neurotrophic factors have been investigated in this regard. This review article discusses the neurodevelopmental roles and therapeutic potential of three dopaminergic neurotrophic factors: glial cell line-derived neurotrophic factor, neurturin and growth/differentiation factor 5. | Shane V.Hegarty Gerard W.O’Keeffe Aideen M.Sullivan | 2014 | Neural Regeneration Research2014，9，19： | 6 |
| 3 | Neurotrophic factor therapy for Parkinson's disease: past, present and future显示文摘One of the greatest unmet needs in the treatment of Parkinson’s disease(PD)is a disease-modifying therapy,which can halt the ongoing degeneration of dopaminergic neurons that is characteristic of this disorder.Current therapies focus on managing symptoms,rather than on addressing their cause.Promising candidates for disease-modifying therapies are the dopaminergic neurotrophic factors(NTFs).NTFs are | Aideen M.Sullivan Gerard W.O'Keeffe | 2016 | Neural Regeneration Research2016，11，2： | 2 |
| 4 | P‐Wave Indices, Distribution and Quality Control Assessment (from the Framingham Heart Study)显示文摘 | Jared W.Magnani Michael J.Mazzini Lisa M.Sullivan MaryAnnWilliamson Patrick T.Ellinor Emelia J.Benjamin | 2010 | Annals of Noninvasive Electrocardiology2010，，1： | 1 |
| 5 | Androgen Deficiency, Meibomian Gland Dysfunction, and Evaporative Dry Eye显示文摘 | DAVID A.SULLIVAN BENJAMIN D.SULLIVAN JAMES E.EVANS FRANKSCHIRRA HIROKOYAMAGAMI MENGLIU STEPHEN M.RICHARDS TOMOSUZUKI DEBRA A.SCHAUMBERG ROSE M.SULLIVAN M. REZADANA | 2006 | Annals of the New York Academy of Sciences2006，，： | 1 |
| 6 | Targeting transcriptional regulators to regenerate midbrain dopaminergic axons in Parkinson's disease显示文摘Introduction:Parkinson’s disease(PD)is a chronic,age-related neurodegenerative disorder that affects 1–2%of the population over the age of 65.PD is characterised by the progressive degeneration of nigrostriatal dopaminergic(DA)neurons.This leads to disabling motor symptoms,due to the striatal DA denervation.Despite decades of research, | Shane V.Hegarty Aideen M.Sullivan Gerard W.O'Keeffe | 2017 | Neural Regeneration Research2017，12，11： | 0 |
| 7 | Growth differentiation factor 5:a neurotrophic factor with neuroprotective potential in Parkinson’s disease显示文摘Parkinson’s disease is the most common movement disorder worldwide,affecting over 6 million people.It is an age-related disease,occurring in 1%of people over the age of 60,and 3%of the population over 80 years.The disease is characterized by the progressive loss of midbrain dopaminergic neurons from the substantia nigra,and their axons,which innervate the striatum,resulting in the characteristic motor and non-motor symptoms of Parkinson’s disease.This is paralleled by the intracellular accumulation ofα-synuclein in several regions of the nervous system.Current therapies are solely symptomatic and do not stop or slow disease progression.One promising disease-modifying strategy to arrest the loss of dopaminergic neurons is the targeted delivery of neurotrophic factors to the substantia nigra or striatum,to protect the remaining dopaminergic neurons of the nigrostriatal pathway.However,clinical trials of two well-established neurotrophic factors,glial cell line-derived neurotrophic factor and neurturin,have failed to meet their primary end-points.This failure is thought to be at least partly due to the downregulation byα-synuclein of Ret,the common co-receptor of glial cell line-derived neurorophic factor and neurturin.Growth/differentiation factor 5 is a member of the bone morphogenetic protein family of neurotrophic factors,that signals through the Ret-independent canonical Smad signaling pathway.Here,we review the evidence for the neurotrophic potential of growth/differentiation factor 5 in in vitro and in vivo models of Parkinson’s disease.We discuss new work on growth/differentiation factor 5’s mechanisms of action,as well as data showing that viral delivery of growth/differentiation factor 5 to the substantia nigra is neuroprotective in theα-synuclein rat model of Parkinson’s disease.These data highlight the potential for growth/differentiation factor 5 as a disease-modifying therapy for Parkinson’s disease. | Susan R.Goulding Jayanth Anantha Louise M.Collins Aideen M.Sullivan Gerard W.O’Keeffe | 2022 | Neural Regeneration Research2022，17，1： | 0 |
| 8 | The Epigenome as a therapeutic target for Parkinson's disease显示文摘Parkinsons disease(PD) is a common,progressive neurodegenerative disease characterised by degeneration of nigrostriatal dopaminergic neurons,aggregation of α-synuclein and motor symptoms.Current dopamine-replacement strategies provide symptomatic relief,however their effectiveness wear off over time and their prolonged use leads to disabling side-effects in PD patients.There is therefore a critical need to develop new drugs and drug targets to protect dopaminergic neurons and their axons from degeneration in PD.Over recent years,there has been robust evidence generated showing that epigenetic dysregulation occurs in PD patients,and that epigenetic modulation is a promising therapeutic approach for PD.This article first discusses the present evidence implicating global,and dopaminergic neuron-specific,alterations in the methylome in PD,and the therapeutic potential of pharmacologically targeting the methylome.It then focuses on another mechanism of epigenetic regulation,histone acetylation,and describes how the histone acetyltransferase(HAT) and histone deacetylase(HDAC) enzymes that mediate this process are attractive therapeutic targets for PD.It discusses the use of activators and/or inhibitors of HDACs and HATs in models of PD,and how these approaches for the selective modulation of histone acetylation elicit neuroprotective effects.Finally,it outlines the potential of employing small molecule epigenetic modulators as neuroprotective therapies for PD,and the future research that will be required to determine and realise this therapeutic potential. | Shane V.Hegarty Aideen M.Sullivan Gerard W.O'Keeffe | 2016 | Neural Regeneration Research2016，11，11： | 0 |
| 9 | 卫生保健改革应促进社会的完善化显示文摘当今的美国社会中充满了各种危机,其根源是社会财富分配不均。因此,卫生改革必须考虑社会和经济问题。改革的目的是向所有公民提供健康保险。由于医疗保健事业是美国经济的煎要组成部分,它影响到人们的思想和道德,只有群众的大力支持,大规模的改革才能成功。文章指出,改革不但应使医疗保健系统成为一个高质量、高效率和有影响力的系统,也应该是一个根治社会弊病的系统,应能促进社会的完善化。 | Joseph M.Sullivan 李馨 | 1993 | 国外医学(医院管理分册)1993，10，4： | 0 |
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