Nootropics与脑认知增强剂
专家视角： 本报告由在药理学和神经科学领域拥有丰富经验的医学研究人员撰写，旨在综合复杂的科学数据，提供一份关于促智药和认知增强剂的全面、权威且基于证据的分析。
促智药与认知增强导论
定义促智药：从 Giurgea 的标准到现代用法
○ 术语起源：“Nootropic”（促智药）一词最早由罗马尼亚心理学家和化学家 Corneliu E. Giurgea 博士在 1972/1973 年提出 。该词源自希腊语 nous（意为“心智”）和 trepein（意为“弯曲/转向”）。最初，Giurgea 用这个词来描述那些能够选择性地激活高级认知功能（如记忆和学习），尤其是在这些功能受损的情况下发挥作用的物质 。吡拉西坦（Piracetam）是 Giurgea 发现的第一种符合这一新类别的物质
○ Giurgea 的原始标准：Giurgea 博士为促智药设定了严格的定义标准 ：
■ 增强学习能力和记忆巩固。
■ 增强已习得行为/记忆对破坏性因素（如缺氧、电休克）的抵抗力。
■ 保护大脑免受各种物理或化学损伤（如巴比妥类药物、东莨菪碱）。
■ 提高大脑皮层/皮层下控制机制的效率（11 中提到促进大脑两半球间信息传递）。
■ 缺乏其他精神药物的常见药理作用（如镇静、运动兴奋），副作用极少且毒性极低。
○ 现代定义与范围蔓延：如今，“促智药”一词的使用范围已大大拓宽，且往往不如 Giurgea 最初定义的那样严谨 。它常被宽泛地用来指代任何声称或意图改善心智技能的天然或合成物质 ，这些技能包括注意力、记忆力、创造力、动机、专注力和觉醒度 。这个宽泛的范畴涵盖了处方药、合成化合物和膳食补充剂 。咖啡因常被认为是世界上消耗量最大的促智药
○ 认知增强的定义：认知增强被定义为通过改进或增强内部或外部信息处理系统，将心智的核心能力放大或扩展至基线水平以上 。这在神经科学领域仍然是一个备受争议的话题
○ 定义的稀释与商业化：从 Giurgea 严格的、以安全为重点的药理学标准，到如今宽泛的营销类别，“促智药”一词经历了显著的语义漂变。Giurgea 的标准 强调神经保护和极低的毒性，同时兼顾认知益处。然而，现代用法 常常包含已知风险的物质（例如处方兴奋剂 ），这些物质可能具有显著的副作用 或其功效证据薄弱 。这种转变与庞大的“健脑”产品市场的兴起相吻合 ，这些产品通常作为膳食补充剂销售，并伴有未经证实的功效声明 。美国食品药品监督管理局（FDA）和联邦贸易委员会（FTC）针对促智药补充剂的误导性营销和欺诈行为发出的警告 突显了这一趋势。最初的科学概念在很大程度上已被商业目的所利用，导致消费者混淆并带来潜在的安全风险 。
○ 缺乏通用标准：目前，对于促智药尚无全球公认的或严格的临床定义 ，这使得该术语变得模糊不清，难以在科学或监管环境中得到一致的应用。虽然 Giurgea 的标准 提供了一个基准，但许多被称为促智药的物质未能完全满足这些标准 。不同的来源对物质的分类也不同（例如，一些来源排除了兴奋剂 ，而另一些则将其包括在内 ）。这种标准定义的缺乏阻碍了清晰的科学交流、有效的监管监督和消费者的理解。现在，“促智药”一词更多地描述了预期用途（认知增强），而不是一个具有明确界定属性的特定药理学类别。
认知增强的历史视角与演变
○ 古老的根源：增强认知能力的愿望可以追溯到几个世纪前 。例如，印度人食用杏仁，古希腊人将迷迭香枝插入头发 ，传统中医使用银杏（Ginkgo Biloba），阿育吠陀医学使用假马齿苋（Bacopa Monnieri）。致幻剂有时在宗教活动中被用于达到被认为能更接近神灵的意识改变状态
○ 启蒙时代与早期合成物：启蒙时代见证了人们对理解人类心智及其潜在增强的兴趣日益增长，认知增强与新兴科学探究之间的联系变得更加明显 。学者和思想家开始仔细记录各种草药和物质，探索它们对心智的影响。咖啡馆成为知识交流的中心，咖啡因的兴奋作用因其能促进警觉性和增强社交互动而备受推崇 。世纪末苯丙胺类药物的合成是促智药发展史上的一个分水岭，标志着合成认知增强剂的出现 。
○ 现代：20世纪见证了处方药的发展，这些药物最初用于治疗认知缺陷（例如，利他林在20世纪50年代用于治疗疲劳/抑郁 ，吡拉西坦在60/70年代用于改善记忆 ）。随后，健康个体开始非适应症使用这些药物 。这包括寻求提高表现的学生、专业人士和军事人员 。天然和合成促智药（通常作为补充剂销售）的市场显著增长
○ 增强实践的连续性：历史上使用物质来影响认知的实践，展示了一个从传统/自然方法到现代药理学干预的连续过程。使用像银杏和假马齿苋这样的植物 代表了早期寻求认知益处的形式。而像吡拉西坦 和兴奋剂 等化合物的科学研究和合成，标志着向更具针对性、更强效（也可能风险更高）的药理学方法的转变。当前的市场格局 反映了这种混合状态，天然补充剂与处方药和新型合成化合物并存，所有这些通常都被归入宽泛的“促智药”范畴。这种演变反映了药理学的更广泛趋势以及社会对性能优化的日益关注。
分类与作用机制
促智药种类繁多，其分类方法也多种多样，反映了这一领域的复杂性。由于缺乏全球统一的定义和标准 ，不同的分类系统侧重于不同的方面，如来源、法律地位、化学结构或作用机制。
○ 按来源分类：这是最广泛的分类方法之一，将促智药分为天然来源和合成来源两大类
天然促智药
包括草药提取物（如银杏、假马齿苋、猴头菇）、氨基酸（如 L-茶氨酸、肌酸）、维生素（如 B 族维生素）、矿物质（如镁）、脂肪酸（如 Omega-3）以及常见的兴奋剂（如咖啡因、尼古丁）。这些通常作为膳食补充剂出售。
合成促智药
指在实验室中创造的化合物，包括处方药和研究性化学品。例子包括拉西坦类（吡拉西坦、阿尼西坦、奥拉西坦、苯基吡拉西坦）、诺培特（Noopept）、莫达非尼（Modafinil）、阿德拉（Adderall）、地阿诺（Deanol）、甲氯芬酯（Meclofenoxate）。它们的可用性各不相同；有些需要处方，有些作为补充剂或研究性化学品出售。
按法律地位分类
这种分类关注物质的监管状态，包括：
处方药
如莫达非尼、阿德拉、利他林、美金刚。这些药物经 FDA 等监管机构批准用于特定医疗目的，但常被健康个体非适应症使用。
非处方药 (OTC)
如咖啡因，在某些地区可能包括吡拉西坦等。
膳食补充剂
通常包含天然成分，如草药、维生素、氨基酸等，监管相对宽松。
未批准药物
通常作为研究性化学品或通过非法渠道销售，如某些拉西坦类药物、芬尼布特（phenibut）等。这些物质的安全性和有效性通常未经证实。
按化学类别分类
这种分类基于物质的化学结构。常见的类别包括：
拉西坦类 (Racetams)
吡咯烷酮衍生物，如吡拉西坦、阿尼西坦、奥拉西坦、苯基吡拉西坦等。
兴奋剂 (Stimulants)
包括苯丙胺类（如阿德拉）、哌醋甲酯（利他林）、尤格罗英类（莫达非尼、阿莫达非尼）。
胆碱能药物 (Cholinergic Agents)
如 Alpha-GPC、胞磷胆碱、地阿诺。
肽类 (Peptides)
如诺培特。
其他类别
如苯乙胺类、GABA能药物、大麻素模拟物、色胺衍生物、哌嗪衍生物等也被提及。
○ 按作用机制分类：这种分类关注药物如何影响大脑功能。一项综述提出了基于作用机制的多个类别（包括作用于受体、酶、离子通道、神经营养因子、再摄取转运体、抗氧化剂、金属螯合剂、疾病修饰药物等），对于机制不明的药物则根据结构（如肽类）或来源（如天然产物）分类。另一项综述则根据 NPSfinder 的分析结果分为若干类。更简单的分类方法包括尤格罗英类、ADHD 药物和促智药补充剂，或者分为经典促智化合物、增加脑代谢物质、胆碱能药物以及具有促智作用的植物及其提取物。
○ 分类的复杂性：被称为促智药的物质种类繁多，性质各异，这使得分类变得困难且常常重叠。目前尚无单一的、普遍接受的分类系统。物质范围从处方兴奋剂到草药提取物和合成肽类。它们的作用机制多样，有时甚至尚不明确。法律地位也因地区而异。这种异质性使得单一、清晰的分类系统难以建立。现有的分类系统反映了不同的侧重点（来源、机制、临床用途），但没有一个能完全捕捉其复杂性。本报告将采用务实的方法，按常见使用类别（处方药、合成非处方药、天然/补充剂）进行分组，并在每个组内讨论具体的作用机制。
促智药靶向的关键神经生物学通路
促智药通过影响大脑中多种复杂的神经生物学通路来发挥其潜在的认知增强作用。了解这些通路对于理解促智药的作用机制、潜在益处和风险至关重要。
主要的神经递质系统包括胆碱能系统、多巴胺能系统、谷氨酸能系统、GABA能系统、5-羟色胺能系统和去甲肾上腺素能系统。其他关键因素还包括神经营养因子、脑代谢（葡萄糖和氧气供应、线粒体功能）、腺苷能调节以及炎症/氧化应激反应。这些系统相互关联，共同构成了认知功能的生物学基础。
○ 胆碱能系统 (Cholinergic System)：乙酰胆碱 (ACh) 是一种对学习、记忆和注意力至关重要的神经递质。许多促智药旨在通过不同机制提高 ACh 水平或活性：
■ 提供 ACh 前体：如胆碱、Alpha-GPC、胞磷胆碱、地阿诺。这些物质在体内转化为胆碱，用于合成 ACh。
■ 抑制 ACh 分解：乙酰胆碱酯酶 (AChE) 会分解 ACh。抑制 AChE（如石杉碱甲）可以提高突触间隙的 ACh 浓度。
■ 调节 ACh 受体：拉西坦类药物和尼古丁等物质可以直接或间接地影响毒蕈碱型或烟碱型乙酰胆碱受体的功能。
■ 增强高亲和力胆碱摄取：某些药物可能促进神经元对胆碱的摄取，从而增加 ACh 的合成。
○ 多巴胺能系统 (Dopaminergic System)：多巴胺参与动机、奖赏、注意力和执行功能。兴奋剂如苯丙胺（阿德拉的主要成分）和哌醋甲酯（利他林）主要通过阻断多巴胺转运体 (DAT) 的再摄取或促进多巴胺（以及去甲肾上腺素）的释放来提高突触间隙的多巴胺水平。莫达非尼也抑制多巴胺再摄取。一些天然促智药，如人参、猴头菇和 L-茶氨酸，也可能刺激多巴胺释放或保护多巴胺通路。
○ 谷氨酸能系统 (Glutamatergic System)：谷氨酸是大脑主要的兴奋性神经递质，在突触可塑性、学习和记忆中起着核心作用。拉西坦类药物（吡拉西坦、阿尼西坦、奥拉西坦）和诺培特被认为或已知能调节谷氨酸受体，特别是 AMPA 和 NMDA 受体。L-茶氨酸也与谷氨酸受体相互作用。通过调节这些受体，促智药可能影响长时程增强 (LTP)，这是学习和记忆的细胞基础。
○ GABA能系统 (GABAergic System)：γ-氨基丁酸 (GABA) 是大脑主要的抑制性神经递质，对于调节神经兴奋性、减少焦虑、促进放松和专注至关重要。
■ 增强GABA活性/水平： L-茶氨酸、某些草药提取物（如缬草、西番莲）。
■ 调节GABA受体： 一些合成化合物（如苯丁胺酸/Phenibut，尽管其促智药分类有争议）直接作用于GABA受体。
■ 认知相关性： 通过降低“神经噪音”，改善信噪比，GABA能系统的调节有助于在不引起镇静的情况下提升专注力和减轻压力相关的认知障碍。
○ 5-羟色胺能系统 (Serotonergic System)：5-羟色胺 (Serotonin) 参与调节情绪、睡眠、食欲、学习和记忆。情绪状态对认知表现有显著影响。
■ 提供5-羟色胺前体： 如5-羟色氨酸 (5-HTP)、L-色氨酸。
■ 调节5-羟色胺受体或再摄取： 虽然很多这类药物被归类为抗抑郁药，但某些具有认知增强的潜力或被用于改善与情绪障碍相关的认知缺陷。一些天然促智药（如圣约翰草，需注意药物相互作用）也可能影响此系统。
■ 认知相关性： 稳定的5-羟色胺水平有助于积极的情绪和心态，这是认知任务高效执行的基础。
○ 去甲肾上腺素能系统 (Noradrenergic System)： 对于警觉性、注意力、压力反应和执行功能至关重要。虽然“多巴胺能系统”中的某些兴奋剂会同时促进多巴胺和去甲肾上腺素的释放，但鉴于其独特的重要性，可以考虑更独立地突出。
■ 调节去甲肾上腺素释放或再摄取： 许多兴奋剂（如哌醋甲酯、苯丙胺类）和莫达非尼都显著影响此系统。一些草药（如红景天）也可能调节去甲肾上腺素水平。
■ 认知相关性： 优化去甲肾上腺素功能可以直接增强专注力、持续注意力及处理复杂任务的能力。
○ 腺苷能系统 (Adenosinergic System)：腺苷是一种抑制性神经调节物质，能促进睡眠和放松。拮抗腺苷受体是提高警觉性和认知表现的常见策略。
■ 腺苷受体拮抗剂： 咖啡因是全球使用最广泛的认知增强剂，其主要机制就是阻断腺苷A1和A2A受体。
■ 认知相关性： 通过抑制腺苷的镇静作用，可以提高觉醒度、反应速度和注意力。
○ 增加脑代谢/血流量：一些物质被认为可以通过扩张脑血管、增加氧气供应和促进葡萄糖利用来改善大脑的能量代谢和血液循环。例子包括长春西汀（Vinpocetine）、尼麦角林（Nicergoline）、银杏叶提取物，以及可能的地阿诺和一般天然促智药。
○ 神经保护/抗氧化作用：许多天然化合物（如银杏、假马齿苋、人参、猴头菇、乙酰左卡尼汀、B 族维生素、镁）和一些合成药物（如吡拉西坦、诺培特、阿尼西坦、奥拉西坦）被认为具有神经保护作用。这通常与抗氧化活性、减少炎症或保护神经元免受兴奋性毒性有关。
○ 调节脑电波/活动：L-茶氨酸能增加与放松警觉状态相关的 α 脑电波。莫达非尼影响特定大脑区域的活动。
○ 神经营养因子：一些物质可能增加脑源性神经营养因子 (BDNF) 或神经生长因子 (NGF) 的水平（例如，诺培特、猴头菇、石杉碱甲、Alpha-GPC、胞磷胆碱、南非醉茄）。这些因子对神经元的生长、存活和可塑性至关重要。
○ 膜流动性/磷脂代谢：拉西坦类药物（吡拉西坦）和胆碱能前体（胞磷胆碱、Alpha-GPC）可能影响细胞膜的结构和功能。例如，吡拉西坦被认为可以恢复老化大脑中降低的膜流动性。
○ 多靶点机制：许多促智药，特别是天然来源的，很可能通过多种相互作用的通路发挥作用，而非单一靶点。例如，假马齿苋和银杏被描述为具有抗氧化、抗炎、胆碱能和促进血流的作用。吡拉西坦则与膜流动性、离子通道调节和神经递质效应相关。这种多靶点作用使得精确机制的研究变得复杂，但也可能解释了其更广泛的效果或协同潜力。这也意味着按单一机制（如“胆碱能”）进行分类可能过于简化。
○ 治疗与增强机制的重叠：促智药所靶向的机制（例如，乙酰胆碱、多巴胺、谷氨酸系统、神经保护）通常与神经退行性疾病或认知障碍中功能失调的通路相同。促智药最初通常是为了治疗阿尔茨海默病、痴呆、中风或 ADHD 等疾病而开发或研究的。这表明，健康个体中认知增强的机制可能涉及对疾病状态下功能失调的相同系统的调节，这引发了关于在健康大脑中改变这些系统的长期影响和潜在风险的问题。
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