Transcranial magnetic stimulation (TMS) reveals decreased efficacy of long-term potentiation-like (LTP-like) neuroplastic mechanisms in Alzheimer's disease (AD). However, it is not yet known whether LTP-like plasticity is also impaired in prodromal AD, or how abnormal TMS measures are related to established AD biomarkers. Here, we investigated the LTP-like response to intermittent theta-burst stimulation in 17 amyloid-positive participants with amnestic mild cognitive impairment (MCI) and 10 cognitively unimpaired controls. Our results showed a lack of LTP-like neuromodulation in MCI compared with controls that was unrelated to quantitative amyloid-beta burden on positron emission tomography. Surprisingly, greater LTP-like response was related to worse memory function in the MCI group, highlighting the complex role of neuroplasticity in the prodromal stages of AD. Overall, our results demonstrate abnormal LTP-like plasticity using intermittent theta-burst stimulation assessment in amyloid-positive participants with MCI. These findings support the potential for development of TMS measures as prognostic markers or therapeutic targets in early-stage symptomatic AD.

中文翻译：

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LTP 样可塑性在淀粉样蛋白阳性遗忘性 MCI 中受损，但与 PET 淀粉样蛋白负荷无关

经颅磁刺激 (TMS) 显示长期增强样 (LTP 样) 神经可塑性机制在阿尔茨海默病 (AD) 中的功效降低。然而，尚不清楚前驱期 AD 中 LTP 样可塑性是否也受到损害，或者异常 TMS 测量与已建立的 AD 生物标志物之间的关系。在这里，我们调查了 17 名患有遗忘型轻度认知障碍 (MCI) 的淀粉样蛋白阳性参与者和 10 名认知未受损的对照组对间歇性 theta 爆发刺激的 LTP 样反应。我们的结果显示，与对照组相比，MCI 中缺乏 LTP 样神经调节，这与正电子发射断层扫描的定量淀粉样蛋白 β 负担无关。令人惊讶的是，在 MCI 组中，更大的 LTP 样反应与更差的记忆功能有关，强调神经可塑性在 AD 前驱阶段的复杂作用。总体而言，我们的结果表明，在患有 MCI 的淀粉样蛋白阳性参与者中使用间歇性 theta-burst 刺激评估异常 LTP 样可塑性。这些发现支持将 TMS 措施发展为早期症状性 AD 的预后标志物或治疗靶标的潜力。