更新于：2024-11-01

CLN3

更新于：2024-11-01

基本信息

别名

Batten disease protein、Batten, Spielmeyer-Vogt disease、Battenin

+ [9]

简介

Mediates microtubule-dependent, anterograde transport connecting the Golgi network, endosomes, autophagosomes, lysosomes and plasma membrane, and participates in several cellular processes such as regulation of lysosomal pH, lysosome protein degradation, receptor-mediated endocytosis, autophagy, transport of proteins and lipids from the TGN, apoptosis and synaptic transmission (PubMed:10924275, PubMed:18817525, PubMed:18317235, PubMed:22261744, PubMed:15471887, PubMed:20850431). Facilitates the proteins transport from trans-Golgi network (TGN)-to other membrane compartments such as transport of microdomain-associated proteins to the plasma membrane, IGF2R transport to the lysosome where it regulates the CTSD release leading to regulation of CTSD maturation and thereby APP intracellular processing (PubMed:10924275, PubMed:18817525). Moreover regulates CTSD activity in response to osmotic stress (PubMed:23840424, PubMed:28390177). Also binds galactosylceramide and transports it from the trans Golgi to the rafts, which may have immediate and downstream effects on cell survival by modulating ceramide synthesis (PubMed:18317235). At the plasma membrane, regulates actin-dependent events including filopodia formation, cell migration, and pinocytosis through ARF1-CDC42 pathway and also the cytoskeleton organization through interaction with MYH10 and fodrin leading to the regulation of the plasma membrane association of Na+, K+ ATPase complex (PubMed:20850431). Regulates synaptic transmission in the amygdala, hippocampus, and cerebellum through regulation of synaptic vesicles density and their proximity to active zones leading to modulation of short-term plasticity and age-dependent anxious behavior, learning and memory (By similarity). Regulates autophagic vacuoles (AVs) maturation by modulating the trafficking between endocytic and autophagolysosomal/lysosomal compartments, which involves vesicle fusion leading to regulation of degradation process (By similarity). Participates also in cellular homeostasis of compounds such as, water, ions, amino acids, proteins and lipids in several tissue namely in brain and kidney through regulation of their transport and synthesis (PubMed:17482562).

关联

靶点

CLN3

作用机制

CLN3表达刺激剂 [+1]

在研机构

The Ohio State University [+2]

原研机构

Nationwide Children's Hospital

在研适应症

神经元蜡样质脂褐质沉积症

非在研适应症-

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期1800-01-20

ABO-201

靶点

CLN3

作用机制

CLN3调节剂

在研机构-

原研机构

Abeona Therapeutics, Inc.

在研适应症-

非在研适应症

神经元蜡样质脂褐质沉积症

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

项与 CLN3 相关的临床试验

NCT03770572 / Active, not recruiting临床1/2期

Phase I/IIa Gene Transfer Clinical Trial for Juvenile Neuronal Ceroid Lipofuscinosis, Delivering the CLN3 Gene by Self-Complementary AAV9

This is a phase 1/2, open-label, single dose, dose-escalation clinical trial to evaluate the safety and efficacy of AT-GTX-502 (previous NCH Code: scAAV9.P546.CLN3) delivered intrathecally into the lumbar spinal cord region of subjects with CLN3 Batten disease.

开始日期2018-11-13

申办/合作机构

Amicus Therapeutics, Inc.

100 项与 CLN3 相关的临床结果

登录后查看更多信息

100 项与 CLN3 相关的转化医学

登录后查看更多信息

0 项与 CLN3 相关的专利（医药）

登录后查看更多信息

807

项与 CLN3 相关的文献（医药）

2024-12-01·Stem Cell Research

Six induced pluripotent stem cell lines from fibroblasts of individuals with CLN3-related conditions

Article

作者: Wassif, Christopher A ; Dang Do, An N. ; Rueda Faucz, Fabio ; Eckhaus, Michael ; O’Mard, Danielle ; Padilla, Cameron ; Villasmil, Rafael ; Zou, Jizhong ; Burkett, Sandra ; Zheng, Wei ; Wassif, Christopher A. ; O'Mard, Danielle ; Dang Do, An N ; Dwojak, Ewelina

Primary fibroblasts from six individuals with CLN3-related conditions were used to generate induced pluripotent stem cell (iPSC) lines CHDTRi001-B, CHDTRi002-B, CHDTRi003-A, CHDTRi004-B, CHDTRi005-A, and CHDTRi006-E through the expression of four reprogramming factors: human OCT3/4, KLF4, SOX2, and c-MYC. The iPSC lines were characterized to confirm their pluripotency via immunocytochemistry, flow cytometry, and teratoma formation. Genomic stability, cell line identity, and CLN3 genotype were confirmed. These iPSC lines may be used as participant-derived experimental models for further investigation of CLN3, a rare, fatal, pediatric, blindness and neurodegenerative lysosomal disorder with no cure.

2024-12-01·Biochemical and Biophysical Research Communications

Increased SNAI2 expression and defective collagen adhesion in cells with pediatric dementia, juvenile ceroid lipofuscinosis

Article

作者: Kim, Hyungkuen ; Bae, Sechul ; Kim, Sung-Jo

Dementia-related neurodegenerative diseases (NDDs), including Alzheimer's disease (AD), are known to be caused by accumulation of toxic proteins. However, the molecular mechanisms that cause neurodegeneration and its biophysical effects on cells remain unclear. In this study, we used juvenile neuronal ceroid lipofuscinosis (JNCL), a pediatric dementia with a clear etiology of mutations in ceroid lipofuscinosis neuronal 3 (CLN3), to explore the changes in cell adhesion, a biophysical process that regulates neuronal development and survival. We used JNCL cerebral organoid gene expression datasets to identify the biological pathways that affect neural development, and found enriched gene expression in the epithelial-mesenchymal transition (EMT) pathway and increased expression of its inducer snail family transcriptional repressor 2 (SNAI2). A cell adhesion assay using lymphoblasts from patients with JNCL revealed defective adhesion to cell culture plates, glass surfaces, collagen type I, and neuroblast-like cells. To determine whether inhibition of EMT could improve the cell adhesion of JNCL lymphoblasts, we used all-trans retinoic acid, a well-known EMT inhibitor and inducer of neural differentiation. In JNCL lymphoblasts, ATRA treatment enhanced adhesion to collagen type I and these effects were abolished by Ca²⁺ chelator. These results provide new insights into the role of CLN3 and cell adhesion in the pathogenesis of NDD.

2024-10-01·Molecular Genetics & Genomic Medicine

Identification of Pathogenic Copy Number Variants in Mexican Patients With Inherited Retinal Dystrophies Applying an Exome Sequencing Data‐Based Read‐Depth Approach

Article

作者: Fabian‐Morales, Gerardo E. ; Montes‐Almanza, Luis ; Zenteno, Juan C. ; Ordoñez‐Labastida, Vianey ; Garcia‐Martínez, Froylan

ABSTRACTBackgroundRetinal dystrophies (RDs) are the most common cause of inherited blindness worldwide and are caused by genetic defects in about 300 different genes. While targeted next‐generation sequencing (NGS) has been demonstrated to be a reliable and efficient method to identify RD disease‐causing variants, it doesn't routinely identify pathogenic structural variant as copy number variations (CNVs). Targeted NGS‐based CNV detection has become a crucial step for RDs molecular diagnosis, particularly in cases without identified causative single nucleotide or Indels variants. Herein, we report the exome sequencing (ES) data‐based read‐depth bioinformatic analysis in a group of 30 unrelated Mexican RD patients with a negative or inconclusive genetic result after ES.MethodsCNV detection was performed using ExomeDepth software, an R package designed to detect CNVs using exome data. Bioinformatic validation of identified CNVs was conducted through a commercially available CNV caller. All identified candidate pathogenic CNVs were orthogonally verified through quantitative PCR assays.ResultsPathogenic or likely pathogenic CNVs were identified in 6 out of 30 cases (20%), and of them, a definitive molecular diagnosis was reached in 5 cases, for a final diagnostic rate of ~17%. CNV‐carrying genes included CLN3 (2 cases), ABCA4 (novel deletion), EYS, and RPGRIP1.ConclusionsOur results indicate that bioinformatic analysis of ES data is a reliable method for pathogenic CNV detection and that it should be incorporated in cases with a negative or inconclusive molecular result after ES.

项与 CLN3 相关的新闻（医药）

2024-01-08

·Science Daily

Possible neuromarker for 'juvenile-onset' Batten disease

Researchers find that an easy-to-measure brain process may be a target or biomarker in measuring treatment outcomes in clinical trials in Batten disease. Early symptoms can be subtle. A child's personality and behavior may change, and clumsiness or stumbling develops between the ages of five and ten. Over time, cognitive impairment sets in, seizures emerge or worsen, vision loss begins, and motor skills decline. This is the course of Batten disease, a progressive inherited disorder of the nervous system that results from mutations to the CLN3 gene. "It is a devastating neurodegenerative disorder of childhood," said John Foxe, PhD, director of the Del Monte Institute for Neuroscience and co-director of the University of Rochester Intellectual and Developmental Disabilities Research Center (UR-IDDRC), "and while it is very rare, it is important to study and understand because it could inform what we know and how we treat it and other related rare diseases." A possible neuromarker In a new study, out today in theJournal of Neurodevelopmental Disorders, Foxe and a team of researchers from the University of Rochester Medical Center may be closer to that goal of understanding. The paper describes how they measured changes in brain function of participants with CLN3 disease, also known as 'juvenile-onset' Batten disease. Researchers found that the functioning of the auditory sensory memory system -- the brain system required for short-term memory recall -- appears to decrease as the disease progresses. They revealed this by utilizing electroencephalographic recordings (EEG) to measure the brain activity of participants with and without Batten disease as they passively listened to simple auditory beeps. The participants simultaneously watched a video of their favorite movie while the brain responses to these beeps were being measured. In the participants with Batten disease, the EEG revealed a decline in the response from the auditory sensory memory system as the disease progressed. There were no significant changes among the other participants. This finding suggests that this easy-to-measure brain process may be a target or biomarker in measuring treatment outcomes in clinical trials. "We needed to find a task that did not require explicit engagement or attention, and this is one of those kinds of tasks," Foxe said. "The brain produces the signal that we're looking at, regardless of whether the participant is paying attention to the beeps or not. It is an objective method that provides new insight into the brain function of a population with varying communication abilities." Leading Batten disease research & treatment There are 12 currently known childhood-onset forms of Batten disease, each genetically distinct from one another, and all significantly impact neurodevelopment. The University of Rochester Batten Center (URBC) is a recognized leader in research and treatment of this condition. URBC is designated a Center of Excellence by the Batten Disease Support and Research Association (BDSRA). The University is a designated Intellectual and Developmental Research Center (IDDRC), and its current principal project is aimed at neuromarker discovery in Batten disease. With several potential gene therapies for Batten disease currently in advanced stages of development, this recent finding continues the mission at URMC to identify biomarkers to evaluate the effectiveness of these experimental treatments. Progressing scientific findings Researchers in the Frederick J. and Marion A. Schindler Cognitive Neurophysiology Lab, where Foxe is co-principal investigator with Edward Freedman, PhD, are using these findings to leverage a Batten disease mouse model. They aim to measure the impact pharmaceuticals have on the auditory perceptual system. Researchers are starting with treatments already on the market for other conditions. "We think this potential biomarker is key to the possibility for us to screen these treatments in the mouse models. The auditory sensory memory marker provides a sensitive measure," Foxe said. "We'll be able to tell you pretty quickly if a treatment is having an impact and know if it is actually changing dynamics -- i.e., whether the system in the brain is improving, what the speed of improvement is, etc. I think that is a big deal." Additional authors include first author Tufikameni Brima, PhD, Edward Freedman, PhD, Kevin Prinsloo, PhD, Heather Adams, PhD, Kuan Hong Wang, PhD, Luke Shaw, and Emma Mantel of the University of Rochester School of Medicine and Dentistry, Erika Augustine, MD, of the Kennedy Krieger Institute, and Jonathan Mink, MD, PhD. This research is supported by the Schmitt Program in Integrative Neuroscience (SPIN) through the Del Monte Institute for Neuroscience pilot program, the National Institute of Neurological Disorders and Stroke, and the Eunice Kennedy Shriver National Institute of Child Health and Human Development.

2023-05-11

·动脉网

成立半年获“未来医疗100强”两类奖项，铂桐医疗以数字医疗赋能医联体闭环疼痛管理

2023年5月6日，“2023未来医疗100强”榜单发布。作为数字医疗领域的优秀企业，铂桐医疗荣获“澎橙奖·年度潜力企业”和价值领域奖。铂桐医疗是国内率先以“癌痛”为切入点的疼痛管理平台，以智能科技为驱动、数据交互为基础、智能算法为核心，赋能医疗机构，闭环解决疼痛。成立不到一年，铂桐医疗打造了软硬件结合的产品矩阵，首创数字医疗赋能的整体疼痛解决方案，核心产品已覆盖全国100多家医疗机构，其数据引擎已积累超过5万例数据。铂桐医疗持续深耕癌症疼痛管理赛道，打造了国内疼痛领域领先的管理平台。构建起从评估、诊疗到管理的服务闭环在5月5日下午举办的数字疗法产业创新实践论坛上，铂桐医疗创始人王杰军教授提到，经过过去10年社会各界的努力，我国总体恶性肿瘤的5年生存率从30.9%提升到40.5%。随着肿瘤总体生存率的提高，肿瘤防控也逐步进入到慢病化管理时代，在持续提高治疗水平的同时，肿瘤患者的生存质量也得到越来越多的关注。其中，“癌痛”作为肿瘤患者最常见的症状之一，严重影响着患者生活质量。王杰军教授在大会上发表主题演讲及圆桌论坛《中国疼痛防控与健康促进战略蓝皮书：中国疼痛医学发展报告（2020）》指出，“我国慢性疼痛患者超过3亿人，且每年以1000万-2000万速度在快速增长，治疗上整体花费约5000亿元。”数据的背后，是疼痛患者及其家庭，乃至全社会承担的巨大压力。面对严峻挑战，政策端明确将在国内推广和执行把“慢性疼痛”“慢性癌痛”等列入疾病诊断的ICD-11的疾病分类系统，为患者收治、医疗质量控制以及医保支付都提供了新契机。铂桐医疗则从产业端发力，致力于打造领先的疼痛管理平台，提高医务人员对肿瘤治疗过程中的疼痛重要性的认知，以及为医务人员提供可执行的标准、可使用的技术工具。已实现B端商业化，将在2023年启动大规模市场拓展BTS （6D疼痛评估系统）是铂桐医疗的核心产品之一。其不仅将原本临床上的多个测试整合起来，而且加入了独有算法，形成一个系统的、多维度的“Total Pain”综合判断，与传统评估问卷BPI相比，BTS评估填写时间更短，受试者使用更方便且更受喜欢；在爆发痛和神经病理痛的预测方面，BTS的准确率均在90%以上。据悉，铂桐医疗预计在2023年发布BTS疼痛评估智能机器人，BTS的大规模临床研究数据即将发表，关于疼痛危象的文章也即将发布，值得期待。铂桐医疗合伙人叶蕾女士曾担任吴阶平医学基金会区域医疗协作体执行秘书，并成功入榜2022年“科创中国”青年创业榜单-长三角G60科创走廊U30，任中国基本建设优化研究会研究员，多年深耕医疗市场领域。铂桐医疗合伙人叶蕾女士她表示，铂桐医疗在B端服务方面已成功实现商业化；同时铂桐医疗在医疗服务商业模式上也做出了成功的探索，通过CPDP医联体实现癌痛质量控制，将产品、系统、设备落地到医疗机构，通过纵向深耕及横向拓展，让铂桐医疗的产品和服务落地更多医院、惠及更多患者，2023年Q3将启动PICU试点建设。身处一线，叶蕾女士对数字医疗行业变化有着清晰感知。她分享到，肿瘤诊疗已从疾病治疗向全生命周期管理转变，因此基于全病程管理的数字医疗是产业重点探索的方向，铂桐医疗的数字医疗全流程整体解决方案正契合了国家和市场对智能化、智慧化的要求。针对数字医疗当前发展现状，她表示，“数字疗法不是黄昏将至，而是涅槃重生”，大浪淘沙之下，经得起市场检验的价值工具始终会被留下。叶蕾女士还介绍到，BTX舒桐多维舒缓仪即将上线，其结合了TENS物理治疗和MBCT心理治疗的方式，是一种综合的疼痛管理方案，具有非成瘾性和非侵入性的优势，安全性高，可以单独使用或联合药物及器械使用，并且可以全面记录疼痛轨迹，跟踪疼痛情况和治疗后变化，更好地评估病情和治疗效果。铂桐医疗的BTX舒桐多维舒缓仪铂桐医疗以数字医疗赋能的整体疼痛解决方案可贯穿病程的诊断、治疗和预后全流程。目前，铂桐医疗的整体疼痛解决方案已形成一个“金字塔”结构。“金字塔”塔底是以BTS多维疼痛评估及支持系统为核心的数字医疗产品矩阵，包含了疼痛诊治的软硬件产品，可延续院外居家疼痛治疗与管理，进行多学科精准诊断，辅助判断病因，并精准、全面评估疼痛状况。铂桐医疗整体解决方案的金字塔结构“金字塔”塔体则是“癌痛规范化能力提升医联体CPDP”项目。这一项目在中国医药卫生事业发展基金会、国家卫健委疼痛质控中心专家、中国临床肿瘤学会支持与康复治疗专家委员会(SCRC)和中国抗癌协会癌症康复与姑息治疗专业委员会(CRPC)的支持下成立，旨在构建癌痛治疗和管理的系统、制度、质控、标准、培训和考核体系，将新理念、新技术和新模式赋能各级医疗机构进行线下落地。“金字塔”塔尖则是疼痛ICU（PAINICU）病房，由镇痛体征检测设备、疼痛评估机器人进行患者生命体征参数收集，经疼痛管理系统PMS、疼痛监测系统PICUS进行数据分析后，输出规范化治疗方案，能够安全、有效地解决疼痛危象、难治性癌痛等难题。除了技术和应用场景的探索，铂桐医疗也构建了创新商业和管理模式——哑铃模式：一端是医疗服务板块；另一端是针对医生群体的培训和临床研究板块；由数据交互管理平台连接，即两端的数据沉淀在平台上，再利用平台数据丰富和升级产品，反馈给两端业务。铂桐医疗的哑铃模式在医疗服务端，铂桐医疗首先利用数字医疗平台产品BTS进行患者评估，基于评估结果建议患者前往线下医疗服务点进行相应治疗；治疗完成后，再通过数字医疗产品BTX进行长期管理。在培训和研究板块，铂桐医疗着力打造疼痛综合管理监测网（CPain），联合医疗机构为医生提供培训教育、进行疼痛质控和真实世界研究等服务。在产品方面，铂桐医疗已经构建起从评估、诊疗到管理的服务闭环。其全流程疼痛管理平台整合了BTS（6D多维疼痛评估系统）、BTC（癌痛多学科咨询系统）、BTX（舒桐多维舒缓仪）。基于此，铂桐医疗还建立了疼痛治疗的标准化临床路径，开发了疼痛管理系统（PMS）、院内疼痛监测系统（PICUS），此外，基于癌痛的大模型(CPM Cancer Pain Foundation Model)已在训练中，帮助各级医疗机构更好地进行同质化的患者疼痛管理。近期推荐声明：动脉网所刊载内容之知识产权为动脉网及相关权利人专属所有或持有。未经许可，禁止进行转载、摘编、复制及建立镜像等任何使用。动脉网，未来医疗服务平台

临床研究

2023-04-26

·生物谷

举铁吧，头脑还能更聪明！Neuroscience新发现：锻炼肌肉有利于增强海马体功能，让大脑更健康！

你有多久没有运动了？在工作外不多的可支配时间里，生活、社交和家庭已然占据了绝大部分，而且似乎也丧失了幼年时一股脑的运动热情，即便我们知道长期坚持运动可以提高心肺、肌肉、骨骼等器官和组织的功能水平，还能缓解焦虑，甚至多种慢性疾病的发生......而且运动的益处也不止于此，近日，美国贝克曼高级科学技术研究所的Justin S. Rhodes和M. Taher A. Saif教授团队在Neuroscience上发表最新成果，该研究显示，锻炼在一定程度上能通过调节星形胶质细胞来增强海马体功能，进一步支持大脑健康。图片来源：doi: 10.1016/j.neuroscience.2023.01.028我们都知道，锻炼有利于大脑健康，目前的解释为，肌肉在收缩时会释放一些因子，这些因子进入体内循环并进入大脑，在大脑中增强海马体功能如神经发生和突触发生。那么，肌肉信号是如何通过海马细胞转导来调节大脑网络活动和突触发育的呢？起初，研究人员在一项小鼠后肢反复电收缩的实验中观察到海马体中新星形胶质细胞的数量增加，这意味着星形胶质细胞对肌肉因子敏感。同时，星形胶质细胞又在血脑屏障的形成中发挥着关键作用，可以将信号传递到大脑。因此，研究人员将收缩肌细胞和海马细胞分离出来进行体外实验。当肌肉细胞成熟时，它们开始自行收缩，将化学信号分子释放到培养基中。将这些含有信号分子的培养基（条件介质，CM）添加到海马神经元和星形胶质细胞的培养体系中，通过免疫荧光、钙成像等技术来观察细胞生长和神经元电信号活动。结果显示，加入含肌肉细胞信号分子的培养基后，海马体神经元表现出了更为频繁和更大强度的电信号，代表神经元迅速生长；几天后神经元形成成熟网络同步发射电信号，就如同大脑一样。此外，作者还发现，肌肉收缩是CM影响海马体所必需的，当使用BTS阻止肌肉收缩时，无论是在常规介质（RM）还是CM中，BTS似乎都直接消除了神经元的同步放电。图1. 肌肉收缩条件介质增加海马神经元活动。图片来源：doi: 10.1016/j.neuroscience.2023.01.028原代海马细胞培养一段时间会形成突触，研究发现，相比于RM，CM更能促进突触发育。对表达S100b（星形胶质细胞标记物）的细胞进行计数量化，从第2天到第9天，星形胶质细胞数量在RM中增加了9.0倍，在CM中增加了10.4倍，这表明来自收缩肌肉的肌肉调节介质诱导星形胶质细胞增殖。星形胶质细胞数量的增加可能通过加强特定突触或削弱其他突触来促进海马网络的成熟。当培养皿中出现新的成熟神经元时表示神经发生，通过对NeuN阳性细胞计数显示，RM和CM在第3天的神经元数量没有显著差异，但CM在第9天的神经元数量比RM多约40%，说明来自收缩肌肉的肌肉调节介质诱导神经发生。图2. 肌肉收缩条件介质加速海马神经元突触发育。图片来源：doi: 10.1016/j.neuroscience.2023.01.028星形胶质细胞作为大脑中接收血液信号的第一反应者，它是如何调节化学信号与海马神经元之间的关系的呢？研究人员从培养体系中去除星形胶质细胞，惊奇的发现神经元活动增强，表明CM增加星形胶质细胞的抑制功能来抵消CM对神经元活动的兴奋作用，从而促进了海马体的可塑性。简单来讲，星形胶质细胞可以阻止海马体本身参与运动反应的过度兴奋，避免神经元失控。图3. 星形胶质细胞释放抑制肌肉介质诱导的神经元活动的因子。图片来源：doi: 10.1016/j.neuroscience.2023.01.028简而言之，运动使肌肉细胞产生的化学信号分子能够让海马神经元兴奋，星形胶质细胞调节神经元活动防止过度兴奋，二者共同促进了大脑功能的健康平衡。另外，海马体是认知，学习和记忆的关键区域，这项研究也为开发认知障碍运动方案提供了新的思路，我们也期待着通过“药物+运动”的合理搭配，让更多的如阿尔兹海默症等认知障碍病患从中获益！天气变暖啦，一起出门动起来吧^_^参考文献：[1] Lee KY, Rhodes JS, Saif MTA. Astrocyte-mediated Transduction of Muscle Fiber Contractions Synchronizes Hippocampal Neuronal Network Development. Neuroscience. 2023 Apr 1; 515:25-36. doi: 10.1016/j.neuroscience.2023.01.028.[2] Ruegsegger GN, Booth FW. Health Benefits of Exercise. Cold Spring Harb Perspect Med. 2018 Jul 2;8(7): a029694. doi: 10.1101/cshperspect. a029694.撰文 | 白露编辑 | cici精彩推荐精彩推荐：1、警惕！BMC：我国学者调查44万人健康数据显示：每周1~3天食用腌菜，死亡风险提升0.32倍！2、长寿的秘密找到了！Nature Aging：我国学者分析300位百岁老人，发现肠道微生物群越像年轻人越健康长寿！3、健康“杀手”帕金森诊断新突破！Lancet子刊最新研究证实：α-突触核蛋白检测有望成为帕金森病筛查新选择4、Cancer Letters：于颖彦教授团队权威综述！从药物筛选到临床试验，类器官应用潜力巨大！5、核桃真的能补脑？《柳叶刀》子刊最新研究：坚持补充核桃可补脑增加预期寿命、降低多种疾病风险！