Domoic acid (DA), the focus of this research, is a marine algal neurotoxin and epileptogen produced by species in the genus Pseudo-nitzschia. DA is found in finfish and shellfish across the globe. The current regulatory limit for DA consumption (20 ppm in shellfish) was set to protect humans from acute toxic effects, but there is a growing body of evidence suggesting that regular consumption of DA contaminated seafood at or below the regulatory limit may lead to subtle neurological effects in adults. The present research uses a translational nonhuman primate model to assess neurophysiological changes after chronic exposure to DA near the regulatory limit. Sedated electroencephalography (EEG) was used in 20 healthy adult female Macaca fascicularis, orally administered 0.075 and 0.15 mg DA/kg/day for at least 10 months. Paired video and EEG recordings were cleaned and a Fast Fourier Transformation was applied to EEG recordings to assess power differences in frequency bands from 1−20 Hz. When DA exposed animals were compared to controls, power was significantly decreased in the delta band (1−4 Hz, p < 0.005) and significantly increased in the alpha band (5−8 Hz, p < 0.005), theta band (9−12 Hz, p < 0.01), and beta band (13−20 Hz, p < 0.05). The power differences were not dose dependent or related to the duration of DA exposure, or subtle clinical symptoms of DA exposure (intentional tremors). Alterations of power in these bands have been associated with a host of clinical symptoms, such as deficits in memory and neurodegenerative diseases, and ultimately provide new insight into the subclinical toxicity of chronic, low-dose DA exposure on the adult primate brain.

软骨藻酸 (DA) 是本研究的重点，是一种由拟菱形藻属物种产生的海洋藻类神经毒素和癫痫原。DA 存在于全球各地的有鳍鱼类和贝类中。目前对 DA 消费量的监管限制（贝类中的 20 ppm）旨在保护人类免受急性毒性作用，但越来越多的证据表明，经常食用等于或低于监管限制的受 DA 污染的海鲜可能会导致轻微的神经系统损害。对成人的影响。本研究使用转化非人类灵长类动物模型来评估长期暴露于接近监管限度的 DA 后的神经生理变化。对 20 名健康成年雌性食蟹猴进行镇静脑电图 (EEG) ，口服 0.075 和 0.15 mg DA/kg/天，持续至少 10 个月。配对视频和脑电图记录被清理，并对脑电图记录应用快速傅里叶变换，以评估 1−20 Hz 频段的功率差异。当暴露于 DA 的动物与对照组相比时，δ 波段（1−4 Hz，p < 0.005）的功率显着下降，而 α 波段（5−8 Hz，p < 0.005）、θ 波段（9−4 Hz，p < 0.005）的功率显着增加。 12 Hz，p < 0.01）和 beta 频段（13−20 Hz，p < 0.05）。功率差异不依赖于剂量，也不与 DA 暴露的持续时间或 DA 暴露的微妙临床症状（故意震颤）相关。这些频带的功率变化与许多临床症状有关，例如记忆缺陷和神经退行性疾病，并最终为慢性低剂量 DA 暴露对成年灵长类动物大脑的亚临床毒性提供了新的见解。