作者：金汉卿
美工：何国红 罗真真
排版：马超
01 引言
延长预期寿命可谓人类公共卫生领域最伟大的成就之一。然而，寿命的增长也伴随与年龄相关的神经系统疾病 (Neurological disorders) 负担不断攀升。神经系统疾病是指发生于中枢或周围神经系统、以感觉、意识、运动等功能受损为主要表现的一类疾病，整体呈现低病死率、高致残率的特点。就在2025年10月14日，世界卫生组织发布了新的《全球神经病学状况报告》1，报告显示神经系统疾病目前影响着全球40%以上的人口——超过30亿人，造成4.35亿伤残调整生命年 (DALY) ，使其成为全球疾病与残疾的主要原因。37种神经系统疾病共导致1180万人死亡、1.62亿年残疾生活年与2.72亿年寿命损失。本文聚焦若干神经系统疾病的治疗前沿，旨在为行业专业人士提供可操作的靶点开发参考。
▲ 图1：影响神经系统疾病的全球负担2
02 阿尔兹海默病
阿尔茨海默病 (Alzheimer’s disease, AD) 是一种以进行性认知障碍为核心表现的中枢神经系统退行性疾病。其病理特征包括淀粉样β (Aβ) 斑块沉积与Tau蛋白异常磷酸化/神经原纤维缠结，并常伴随神经炎症与突触功能障碍。近年，基于脑脊液/影像的病理分层逐步延伸至血液标志物 (如血浆p tau217) ，为早期识别与入组提供更可及的工具。
▲ 图2：阿尔茨海默病的病理机制3
目前的治疗以对症药物 (胆碱酯酶抑制剂与NMDA受体拮抗剂) 和在早期人群中使用的疾病修饰疗法为主。抗Aβ单抗方面，lecanemab (Leqembi) 已在2023年获FDA批准，而donanemab (Kisunla) 也于2024年获FDA批准用于早期症状性AD (MCI/轻度痴呆) 并按月静脉给药。临床实践通常需要影像/体液证据确认Aβ阳性，并在治疗过程中进行MRI监测以管理ARIA。
• 药物前沿进展聚焦三条主线：
抗Aβ策略升级：已上市抗体在早期人群显示减缓进展的临床获益。为实现更高的皮层暴露，罗氏开发Brainshuttle技术，通过偶联可结合转铁蛋白受体 (TfR) 的模块，显著提高穿透BBB能力与脑内分布。
抗Tau与联合方案：多款抗Tau通路药物推进中。尽管单药结果不积极，但与Aβ清除形成序贯/联合方案，有望影响下游神经退行改变。
炎症抑制与精准分层：围绕神经炎症的多靶点布局逐步成形。例如选择性中和可溶性TNF的XPro™/XPro1595：II期MINDFuL总体未达主要终点，但在炎症生物标志物富集的早期AD亚组出现认知、行为与生物学端点的获益信号，且安全性良好，提示“炎症表型分层”的精准用药方向。
▲ 图3：阿尔茨海默病的在研药物靶点汇总
03 帕金森病
帕金森病 (Parkinson’s disease, PD) 是一种影响中枢神经系统、以运动系统受累为主的慢性神经退行性疾病，症状通常缓慢进展。静止性震颤、肌强直、运动迟缓与步态异常常见于早期，也可伴随认知与行为改变。病理学上，以黑质多巴胺能神经元丢失及细胞内α‑突触核蛋白聚集为特征；早期退变多局限于腹外侧黑质，随病程推进而扩展。路易体主要由聚集的α‑突触核蛋白组成，病变通常自脑干胆碱能/单胺能神经元与嗅觉系统起始，随后累及边缘系统和新皮质。
▲ 图4：帕金森病的病理机制4
现行治疗方面，左旋多巴及多巴胺替代治疗仍为金标准。早期可用左旋多巴单药，或联合多巴胺激动剂 (如罗匹尼罗、普拉克索、罗替戈汀) 及MAO‑B抑制剂 (如司来吉兰、雷沙吉兰) 。与早期左旋多巴单药相比，早期启用多巴胺激动剂对长期残疾与生活质量并无显著优势。对出现“开-关”波动者，常通过缩短左旋多巴给药间隔，联合COMT抑制剂 (恩他卡朋、阿匹卡朋) 和/或MAO-B抑制剂 (司来吉兰、雷沙吉兰、沙芬酰胺、唑尼沙胺) ，并调增多巴胺激动剂；若出现异动症，可加用金刚烷胺；部分合适人群可考虑设备辅助治疗以缩短“关”期并改善运动障碍。
• 药物/技术前沿主要包括：
靶向α‑突触核蛋白的被动免疫：临床前可改善病理与行为。两项大型早期PD试验 (SPARK/cinpanemab与PASADENA/prasinezumab) 虽未达主要终点，PASADENA显示运动进展减缓趋势。基于2b期PADOVA及其OLE与PASADENA长随，罗氏已推进prasinezumab进入III期。
LRRK2降解/抑制策略：LRRK2为公认关键靶点。2025年10月8日，Arvinas公布ARV‑102 (LRRK2降解剂) I期积极数据，显示良好的脑脊液暴露与显著的靶蛋白下调 (外周>90%，脑脊液>50%) ，并伴随pRab10与尿BMP等下游生物标志物降低。
基因治疗：AAV2‑GAD向丘脑底核递送在晚期PD中证实安全并带来治疗侧改善；AAV2‑AADC在壳核过表达可增强左旋多巴转化，6个月UPDRS (用药/停药) 约三成改善且用药剂量下降，但4年随访提示临床收益逐步回归基线，提示需进一步优化递送与联合策略。
▲ 图5：帕金森病的在研药物靶点汇总
04 中风
中风 (Stroke，脑卒中) 包括缺血性与出血性两大类，其中以缺血性为主。其发病机制中，缺血造成的级联反应涉及多种中枢神经系统细胞：在缺血核心，神经元发生形态改变，细胞体与轴突消失；小胶质细胞、星形胶质细胞亦随之发生反应性改变。缺血后BBB通透性增加，多种免疫细胞 (白细胞、单核细胞、巨噬细胞) 浸润病灶区，释放神经毒性或神经营养因子，对受损脑组织产生既可能保护亦可能有害的影响。
▲ 图6：脑卒中的病理机制5
现行治疗策略强调“急性再灌注+二级预防”两端发力。针对急性期，发病4.5小时内静脉溶栓仍为基础。除阿替普酶外，多项指南与综述支持替奈普酶 (TNK) 0.25 mg/kg在部分场景作为替代选择；对大血管闭塞患者，借助灌注成像选择性入组，机械取栓时间窗可拓至6–24小时。针对二级预防，小卒中/高危TIA人群的短期双联抗血小板 (阿司匹林+氯吡格雷) 获益主要集中在起始后21天内；合并房颤者以口服抗凝 (优选DOACs) 为一线，无法长期抗凝者可考虑左心耳封堵 (LAAO) 作为替代或补充方案。
• 药物/技术前沿主要体现在：
靶向药：
1. glenzocimab (抗GPVI) 旨在在降低血栓形成的同时控制出血风险；
2. 3K3A‑APC兼具神经与血管保护，早期研究显示良好安全性与出血相关指标改善信号；
3. nerinetide (PSD‑95抑制肽) 总体结论中性，但在未合用tPA或特定流程亚群显现潜在获益，提示存在人群与流程依赖性。
细胞与基因治疗：
1. SB623 (基因改造间充质基质细胞) 用于慢性期功能重建显示上肢运动量表改善且安全性良好；
2. MultiStem (同种异体MAPC) 在18–36小时给药窗内安全可行，关键III期验证持续；
3. AAV递送 (如VEGF/神经营养因子/抗炎因子) 临床前证据积极，但跨BBB的安全与递送效率仍是转化瓶颈。
▲ 图7：脑卒中的在研药物靶点汇总
05 其他神经系统疾病及治疗前沿
除AD、PD与中风外，神经系统疾病还包括多发性硬化 (MS)、视神经脊髓炎谱系疾病 (NMOSD) 、肌萎缩侧索硬化 (ALS)、重症肌无力 (gMG) 、偏头痛等。随着靶向药与技术平台的演进，越来越多的创新疗法为不同疾病带来新的治疗希望：
NMOSD：已有三条机制获批——补体C5抑制剂 (依库珠单抗/拉夫珠单抗) 、抗CD19 (伊妥珠单抗/inebilizumab) 、抗IL‑6R (沙妥利珠单抗/satralizumab) 。
偏头痛：中枢敏化与CGRP通路为关键机制。美国头痛学会已将CGRP疗法 (艾伦单抗/芙马珠单抗/加拉单抗/艾普替单抗) 纳入一线预防选项。
gMG：FcRn拮抗剂 (efgartigimod、rozanolixizumab) 与补体C5抑制剂 (eculizumab、ravulizumab) 确立了分子靶向治疗范式，显著改善症状、加速缓解。
• 基因疗法亦加速进入临床：
亨廷顿病 (HD)：等位基因选择性ASO (WVE‑003) 实现突变HTT下调且安全性可接受；AMT‑130 (AAV‑miHTT) I/II期长随提示疾病进展减缓信号。
难治性癫痫：ASO上调SCN1A (zorevunersen/STK‑001) 在早期研究显示发作频率下降与行为/认知改善信号；基因调控疗法ETX101 (AAV9) 在SCN1A+德拉维特综合征进入I/II期；抑制性中间神经元细胞疗法NRTX‑1001在成人MTLE一期呈现发作显著降低与良好耐受性。
脊髓性肌萎缩 (SMA)：已建立三大治疗支柱——ASO (nusinersen) 、基因疗法 (AAV9‑SMN1，onasemnogene abeparvovec) 与口服小分子剪接调节剂 (risdiplam) 。
06 神经系统疾病治疗总结
神经系统疾病呈“低病死、高致残”特征，已成全球疾病负担首因。治疗正由对症控制走向“疾病修饰+精准分层”。阿尔茨海默病方面，抗Aβ单抗 (lecanemab、donanemab) 在早期人群证实减缓进展，血液标志物与穿越BBB的递送技术 (如Brainshuttle) 加速落地，抗Tau与抗炎 (如选择性中和可溶性TNF) 成为重要补充。帕金森病仍以多巴胺替代为基石，但围绕α-突触核蛋白的免疫、LRRK2抑制/降解与基因治疗正在逼近关键验证。中风治疗两端发力：急性期强调再灌注 (TNK与晚窗机械取栓) ，二级预防重视分型与个体化 (短期DAPT、DOACs、LAAO) 。除AD/PD/中风外，NMOSD、gMG、偏头痛已形成明确分子靶向范式；HD、癫痫、SMA等病种的基因/细胞疗法进展迅速。
• 针对神经系统疾病的未来治疗方向将聚焦于：
① 跨BBB递送与长效化——TfR介导、脑内暴露定量学、皮下长效制剂；
② 基因治疗——AAV/ASO精准调控与免疫规避，提升持续表达与安全窗；
③ AOC药物——抗体-寡核苷酸偶联，实现细胞/区域特异输送与基因沉默、上调或剪接校正，为难治性癫痫、遗传性运动障碍等提供新解。
Sanyou 10th Anniversary: Therapeutic Advances in Neurological Disorders
01 Introduction
Extending life expectancy is one of humanity’s greatest public-health achievements. Yet longer lives come with a steadily rising burden of age-related neurological disorders. Neurological disorders—conditions of the central or peripheral nervous system characterized primarily by impairments of sensation, consciousness, and movement—generally have low case-fatality but high disability rates. On October 14, 2025, the World Health Organization released a new Global Status Report on Neurology1, estimating that neurological disorders currently affect over 40% of the world’s population—more than 3 billion people—and account for 435 million disability-adjusted life years (DALYs), making them the leading cause of disease and disability worldwide. Across 37 neurological conditions, there were 11.8 million deaths, 162 million years lived with disability, and 272 million years of life lost. This article highlights therapeutic frontiers across selected neurological diseases to provide actionable target ideas for R&D professionals.
▲ Fig. 1 Global burden of conditions affecting the nervous system2
02 Alzheimer’s Disease
Alzheimer’s disease (AD) is a progressive, degenerative disorder of the central nervous system whose core clinical feature is cognitive decline. Pathology includes extracellular amyloid-β (Aβ) plaque deposition and abnormal phosphorylation of tau protein/neurofibrillary tangles, often accompanied by neuroinflammation and synaptic dysfunction. In recent years, pathology-based stratification via CSF/imaging has extended to blood biomarkers (e.g., plasma p-tau217), providing more accessible tools for early identification and trial enrollment.
▲ Fig. 2 Pathology of Alzheimer’s disease3
• Current therapies
Management combines symptomatic agents (cholinesterase inhibitors and the NMDA receptor antagonist memantine) with disease-modifying therapy initiated in early-symptomatic populations. Among anti-Aβ monoclonal antibodies, lecanemab (Leqembi) received traditional FDA approval in 2023 with labeling that emphasizes ARIA risk and APOE ε4 stratification; donanemab (Kisunla) was approved in 2024 for early symptomatic AD (MCI/mild dementia) and is administered as monthly IV infusions. In clinical practice, Aβ positivity is typically confirmed by imaging or fluid biomarkers, and MRI monitoring is used during treatment to manage ARIA.
• Frontline R&D themes
Upgrading anti-Aβ strategies. Marketed antibodies show clinically meaningful slowing in early-stage populations. To achieve higher cortical exposure, Roche is developing Brainshuttle technology by coupling to transferrin receptor (TfR)–binding modules, markedly improving BBB penetration and brain distribution.
Anti-tau and combination/sequencing. Multiple programs targeting tau pathways are advancing. Although monotherapy results have been mixed, pairing with Aβ clearance in sequential/combination regimens may modulate downstream neurodegeneration.
Inflammation control with precise stratification. A growing multi-target portfolio focuses on neuroinflammation. For example, selective neutralization of soluble TNF with XPro™/XPro1595 missed the primary endpoint in the phase II MINDFuL study overall, but showed signals of benefit across cognitive, behavioral, and biomarker endpoints in an inflammation-enriched early-AD subgroup with good safety—supporting “inflammatory phenotype stratification” for precision use.
▲ Fig. 3 Drug targets under development for Alzheimer’s disease
03 Parkinson’s Disease
Parkinson’s disease (PD) is a chronic neurodegenerative disorder primarily affecting the motor system with typically slow progression. Early features include resting tremor, rigidity, bradykinesia, and gait disturbance, often with cognitive/behavioral changes. Pathology features loss of dopaminergic neurons in the substantia nigra and intracellular α-synuclein aggregation; early degeneration is often localized to the ventrolateral substantia nigra and expands with disease. Lewy bodies are mainly composed of aggregated α-synuclein, with lesions commonly starting in brainstem cholinergic/monoaminergic neurons and the olfactory system, then involving limbic structures and neocortex.
▲ Fig. 4 Pathology of Parkinson’s disease4
• Current therapies
There is no established disease-modifying therapy. Levodopa and dopamine replacement remain the gold standard. Early treatment can be levodopa monotherapy or combined with dopamine agonists (e.g., ropinirole, pramipexole, rotigotine) and MAO-B inhibitors (e.g., selegiline, rasagiline). Compared with early levodopa monotherapy, starting dopamine agonists early shows no clear advantage for long-term disability or quality of life. For “on–off” fluctuations, clinicians often shorten levodopa dosing intervals, add COMT inhibitors (entacapone, opicapone) and/or MAO-B inhibitors (selegiline, rasagiline, safinamide, zonisamide), and titrate dopamine agonists; amantadine may be added for dyskinesia. Device-aided therapies can be considered in selected patients to reduce “off” time and improve motor complications.
• Frontline R&D themes
Passive immunotherapy against α-synuclein. Preclinical data show improvements in pathology and behavior. Although two large early-PD trials (SPARK/cinpanemab and PASADENA/prasinezumab) missed primary endpoints, PASADENA showed a trend toward slower motor progression. Based on phase 2b PADOVA and its OLE plus long-term PASADENA follow-up, Roche has advanced prasinezumab into phase III.
LRRK2 inhibition/degradation. LRRK2 is a validated target. On October 8, 2025, Arvinas reported positive phase I data for the LRRK2 degrader ARV102, showing good CSF exposure and robust target knock-down (>90% peripherally, >50% in CSF) with reductions in downstream biomarkers (pRab10 and urinary BMP).
Gene therapy. AAV2-GAD delivery to the subthalamic nucleus showed safety and improvement on the treated side in advanced PD; AAV2-AADC overexpression in the putamen enhances levodopa conversion, producing ~30% improvement in UPDRS (on/off medication) at 6 months and reduced medication needs, though 4-year follow-up suggests benefits trend back toward baseline—highlighting the need to optimize delivery and combinations.
▲ Fig. 5 Drug targets under development for Parkinson’s disease
04 Stroke
Stroke comprises ischemic and hemorrhagic types, with ischemic stroke predominating. The ischemic cascade involves multiple CNS cell types: in the core, neurons undergo morphological changes with loss of soma and axons; microglia and astrocytes also react. Post-ischemia, BBB permeability increases; leukocytes, monocytes, and macrophages infiltrate the lesion, releasing either neurotoxic or neurotrophic factors with potentially protective or harmful effects on injured brain tissue.
▲ Fig. 6 Pathology of stroke5
• Current strategies
Management emphasizes both acute reperfusion and secondary prevention. For the acute phase, IV thrombolysis within 4.5 hours remains foundational. Beyond alteplase, guidelines and reviews support tenecteplase (TNK) 0.25 mg/kg as an alternative in selected scenarios. For large-vessel occlusion, perfusion-imaging–guided selection enables mechanical thrombectomy in the 6–24 hour window. For secondary prevention, short-term dual antiplatelet therapy (aspirin + clopidogrel) in minor stroke/high-risk TIA confers most of its benefit within 21 days of initiation. In patients with atrial fibrillation, oral anticoagulation (preferably DOACs) is first-line; when long-term anticoagulation is unsuitable, left atrial appendage occlusion (LAAO) can be considered as an alternative or adjunct.
• Frontline R&D themes
Targeted agents：
1. glenzocimab (anti-GPVI): aims to curb thrombosis while controlling bleeding risk.
2. 3K3A-APC: offers neuro- and vasculo-protection; early studies suggest good safety and favorable bleeding-related signals.
3. nerinetide (PSD-95 inhibitor peptide): neutral overall, but potential benefit in subgroups not receiving tPA or under specific workflow conditions—suggesting population/process dependence.
Cell and gene therapies：1. SB623 (gene-modified mesenchymal stromal cells) for chronic-phase functional recovery improved upper-limb scales with good safety.
2. MultiStem (allogeneic MAPC) appears safe/feasible with dosing at 18–36 hours; pivotal phase III confirmation is ongoing.
3. AAV delivery (e.g., VEGF/neurotrophic/anti-inflammatory factors) shows encouraging preclinical evidence, but safe and efficient BBB crossing remains a translational bottleneck.
▲ Fig. 7 Drug targets under development for stroke
05 Other Neurological Diseases and Therapeutic Frontiers
Beyond AD, PD, and stroke, neurological disorders include multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), amyotrophic lateral sclerosis (ALS), generalized myasthenia gravis (gMG), migraine, and more. With the evolution of targeted drugs and platform technologies, an expanding array of innovative therapies is delivering new hope:NMOSD: Three approved mechanisms—complement C5 inhibitors (eculizumab/ravulizumab), anti-CD19 (inebilizumab), and anti-IL-6R (satralizumab).
Migraine: Central sensitization and the CGRP pathway are key. The American Headache Society now lists CGRP-pathway therapies (erenumab, fremanezumab, galcanezumab, eptinezumab) as first-line options for prevention.
gMG: FcRn antagonists (efgartigimod, rozanolixizumab) and complement C5 inhibitors (eculizumab, ravulizumab) have established a molecularly targeted paradigm, improving symptoms and accelerating remission.
• Gene and cell therapies accelerating into the clinicHuntington’s disease (HD): Allele-selective ASO WVE-003 lowers mutant HTT with acceptable safety; AMT-130 (AAV-miHTT) phase I/II long-term follow-up suggests signals of slowed disease progression.
Refractory epilepsy: ASO zorevunersen/STK-001 upregulates SCN1A with early signals of seizure reduction and behavioral/cognitive improvement; gene-regulation therapy ETX101 (AAV9) has entered phase I/II for SCN1A-positive Dravet syndrome; an inhibitory interneuron cell therapy NRTX1001 in adult MTLE phase I shows marked seizure reduction with good tolerability.
Spinal muscular atrophy (SMA): A tri-pillar framework is established—ASO (nusinersen), gene therapy (onasemnogene abeparvovec, AAV9-SMN1), and oral small-molecule splicing modulation (risdiplam).
06 Summary of Therapeutic Directions
Neurological disorders feature low mortality but high disability , now the top contributor to global disease burden. Treatment is shifting from symptomatic control to disease modification with precise stratification.AD: Anti-Aβ antibodies (lecanemab, donanemab) slow progression in early populations; blood biomarkers and BBB-shuttling technologies (e.g., Brainshuttle) are moving into practice. Anti-tau and anti-inflammatory approaches (e.g., selective neutralization of soluble TNF) are important complements.
PD: Dopamine replacement remains foundational, while α-synuclein immunotherapy, LRRK2 inhibition/degradation, and gene therapy approach key validation milestones.
Stroke: Dual-pronged care—acute reperfusion (TNK and extended-window thrombectomy) and individualized secondary prevention (short-term DAPT, DOACs, LAAO).
Others: NMOSD, gMG, and migraine already have clear targeted paradigms; gene/cell therapies are rapidly advancing in HD, epilepsy, SMA, and beyond.
• Future priorities will focus on1. Cross-BBB delivery and durability—TfR-mediated shuttles, quantitative CNS exposure, and long-acting subcutaneous formulations.
2. Gene therapy—AAV/ASO precision control with immune evasion, enhancing persistence and safety margins.
3. AOC (antibody–oligonucleotide conjugates)—cell/region-specific delivery enabling gene silencing, up-regulation, or splice correction, offering new solutions for refractory epilepsy, inherited movement disorders, and more.
▶ Ref
1. Global status report on neurology
2. GBD 2021 Nervous System Disorders Collaborators. Global, regional, and national burden of disorders affecting the nervous system, 1990-2021: a systematic analysis for the Global Burden of Disease Study 2021. Lancet Neurol. 2024;23(4):344-381. doi:10.1016/S1474-4422(24)00038-3
3. Kamatham PT, Shukla R, Khatri DK, Vora LK. Pathogenesis, diagnostics, and therapeutics for Alzheimer's disease: Breaking the memory barrier. Ageing Res Rev. 2024;101:102481. doi:10.1016/j.arr.2024.102481
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三优生物是一家以“让天下没有难做的创新生物药”为使命，以超万亿分子库和智能科技驱动的生物医药高科技企业。
公司致力于打造全球顶尖的原创新药创新工场。公司以智能超万亿分子库（AI-STAL）为核心；以干湿结合、国际领先的创新生物药智能化及一体化研发平台为依托；以多样化的业务模式推动全球创新药物的研发及产业化。
公司总部位于中国上海，在亚洲、北美洲、欧洲等多地建立了业务中心，形成了全球化的业务网络，现有投产及布局的研发及GMP场地20000多平方米。
公司已与全球2000多家药企、生技公司等建立了良好的合作关系，已赋能1200多个新药研发项目；已完成50多个合作研发项目，其中10多个协同研发项目已推至IND及临床研发阶段。
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