Birba Agustina, Hesse Eugenia, Sedeño Lucas, Mikulan Ezequiel P, García María Del C, Ávalos Juan, Adolfi Federico, Legaz Agustina, Bekinschtein Tristán A, Zimerman Máximo, Parra Mario, García Adolfo M, Ibáñez Agustín
Laboratory of Experimental Psychology and Neuroscience (LPEN), Institute of Cognitive and Translational Neuroscience (INCyT), INECO Foundation, Favaloro UniversityBuenos Aires, Argentina.
National Scientific and Technical Research Council (CONICET)Buenos Aires, Argentina.
Front Aging Neurosci. 2017 Jun 8;9:178. doi: 10.3389/fnagi.2017.00178. eCollection 2017.
Recent works evince the critical role of visual short-term memory (STM) binding deficits as a clinical and preclinical marker of Alzheimer's disease (AD). These studies suggest a potential role of posterior brain regions in both the neurocognitive deficits of Alzheimer's patients and STM binding in general. Thereupon, we surmised that stimulation of the posterior parietal cortex (PPC) might be a successful approach to tackle working memory deficits in this condition, especially at early stages. To date, no causal evidence exists of the role of the parietal cortex in STM binding. A unique approach to assess this issue is afforded by single-subject direct intracranial electrical stimulation of specific brain regions during a relevant cognitive task. Electrical stimulation has been used both for clinical purposes and to causally probe brain mechanisms. Previous evidence of electrical currents spreading through white matter along well defined functional circuits indicates that visual working memory mechanisms are subserved by a specific widely distributed network. Here, we stimulated the parietal cortex of a subject with intracranial electrodes as he performed the visual STM task. We compared the ensuing results to those from a non-stimulated condition and to the performance of a matched control group. In brief, direct stimulation of the parietal cortex induced a selective improvement in STM. These results, together with previous studies, provide very preliminary but promising ground to examine behavioral changes upon parietal stimulation in AD. We discuss our results regarding: (a) the usefulness of the task to target prodromal stages of AD; (b) the role of a posterior network in STM binding and in AD; and
近期研究表明，视觉短期记忆（STM）结合缺陷作为阿尔茨海默病（AD）临床和临床前标志物具有关键作用。这些研究表明，后脑区域在阿尔茨海默病患者的神经认知缺陷以及一般STM结合中可能发挥潜在作用。因此，我们推测刺激顶叶后皮质（PPC）可能是解决这种情况下工作记忆缺陷的成功方法，尤其是在早期阶段。迄今为止，尚无关于顶叶皮质在STM结合中作用的因果证据。一种评估此问题的独特方法是在相关认知任务期间对特定脑区进行单受试者直接颅内电刺激。电刺激已用于临床目的并用于因果探究脑机制。先前有证据表明电流沿明确的功能回路通过白质传播，这表明视觉工作记忆机制由特定的广泛分布网络支持。在此，我们在一名受试者执行视觉STM任务时用颅内电极刺激其顶叶皮质。我们将随后的结果与未刺激条件下的结果以及匹配对照组的表现进行了比较。简而言之，直接刺激顶叶皮质可使STM有选择性地改善。这些结果与先前的研究一起，为研究AD患者顶叶刺激后的行为变化提供了非常初步但有前景的基础。我们讨论了关于以下方面的结果：（a）该任务对AD前驱期的针对性作用；（b）后脑网络在STM结合和AD中的作用；以及
