基于对 GRIN2A 的分析，研究团队在 121 名受试者中鉴定出 85 名携带基因变异者，其中 23 名（约 27％）发展出明确精神疾病，显示单基因变异即可显著提高风险。数据指出该突变削弱 NMDA 受体活性，进而扰动神经讯号传递，并挑战对精神疾病必然为多基因累积效应的传统假设。患者的症状高度精神科专一性，强化了遗传因子在病程中的主导性。

GRIN2A 编码之 GluN2A 蛋白为神经电讯号传递与学习、记忆、语言及脑发育的核心元件。变异造成的 NMDA 功能下降已在先前以 L-serine 补充进行的小型试验中呈现可逆性；四名精神分裂症患者在干预后出现幻觉消失、被害观念缓解与行为改善，但作者强调需以随机、前瞻、双盲方法验证其效力。

精神分裂症全球患者约 2,300 万人，占总人口 0.29％；成人比率增至 0.43％，即每 233 人中约 1 人。症状、危险因子与治疗机制已有相当理解，但病因仍未被单一模型完全解释，且高危族群中存在强烈变异性。由于即使双亲皆受诊断，后代表现仍不一致，目前亦无可明确阻断疾病起始的方案。

Based on analysis of GRIN2A, researchers identified 85 carriers among 121 subjects, with 23 (approximately 27%) developing clear mental illness, demonstrating that a single-gene variant can markedly elevate risk. Data show the mutation weakens NMDA receptor activity, disrupting neural signaling and challenging the prevailing assumption that mental disorders arise only from polygenic accumulation. Patients exhibited strictly psychiatric symptoms, reinforcing the dominant role of genetic factors.

GRIN2A encodes the GluN2A protein, essential for neural signal transmission and for learning, memory, language, and brain development. NMDA dysfunction produced by the variant showed reversibility in a prior small L-serine intervention trial; four schizophrenia patients exhibited disappearance of hallucinations, remission of paranoia, and behavioral improvement, though authors emphasize that randomized, prospective, double-blind confirmation is required.

Schizophrenia affects about 23 million people globally, or 0.29% of the population; the adult rate rises to 0.43%, roughly 1 in 233 individuals. Symptoms, risk factors, and therapeutic mechanisms are well characterized, yet no single causal model accounts for observed variability, and high-risk individuals differ widely in outcomes. Even with two diagnosed parents, onset is inconsistent, and no definitive prevention strategy exists.