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Estimating Memory Deterioration Rates Following Neurodegeneration and Traumatic Brain Injuries in a Hopfield Network Model

机译:在Hopfield网络模型中估算神经变性和颅脑外伤后的记忆退化率

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Neurodegenerative diseases and traumatic brain injuries (TBI) are among the main causes of cognitive dysfunction in humans. At a neuronal network level, they both extensively exhibit focal axonal swellings (FAS), which in turn, compromise the information encoded in spike trains and lead to potentially severe functional deficits. There are currently no satisfactory quantitative predictors of decline in memory-encoding neuronal networks based on the impact and statistics of FAS. Some of the challenges of this translational approach include our inability to access small scale injuries with non-invasive methods, the overall complexity of neuronal pathologies, and our limited knowledge of how networks process biological signals. The purpose of this computational study is three-fold: (i) to extend Hopfield's model for associative memory to account for the effects of FAS, (ii) to calibrate FAS parameters from biophysical observations of their statistical distribution and size, and (iii) to systematically evaluate deterioration rates for different memory-recall tasks as a function of FAS injury. We calculate deterioration rates for a face-recognition task to account for highly correlated memories and also for a discrimination task of random, uncorrelated memories with a size at the capacity limit of the Hopfield network. While it is expected that the performance of any injured network should decrease with injury, our results link, for the first time, the memory recall ability to observed FAS statistics. This allows for plausible estimates of cognitive decline for different stages of brain disorders within neuronal networks, bridging experimental observations following neurodegeneration and TBI with compromised memory recall. The work lends new insights to help close the gap between theory and experiment on how biological signals are processed in damaged, high-dimensional functional networks, and towards positing new diagnostic tools to measure cognitive deficits.
机译:神经退行性疾病和脑外伤(TBI)是人类认知功能障碍的主要原因。在神经元网络水平上,它们都广泛表现出局灶性轴突肿胀(FAS),这反过来又损害了穗序列中编码的信息,并可能导致严重的功能缺陷。基于FAS的影响和统计,目前尚无令人满意的定量预测记忆编码神经元网络数量下降的指标。这种转换方法的一些挑战包括我们无法使用非侵入性方法治疗小规模损伤,神经元病理的整体复杂性以及我们对网络如何处理生物信号的了解有限。这项计算研究的目的包括三个方面:(i)扩展用于关联记忆的Hopfield模型以说明FAS的影响;(ii)从其统计分布和大小的生物物理观测值中校准FAS参数,以及(iii)系统地评估不同记忆调用任务的恶化率与FAS损伤的关系。我们计算出人脸识别任务的恶化率,以说明高度相关的内存以及随机,不相关的内存(其大小在Hopfield网络的容量限制范围内)的判别任务。虽然预计任何受损网络的性能都会随着受损而降低,但我们的结果首次将记忆调用能力与观察到的FAS统计数据联系起来。这样就可以对神经元网络内不同阶段的脑部疾病的认知能力下降进行合理的估计,从而将神经退行性变和TBI后的实验观察与受损的记忆记忆联系起来。这项工作提供了新的见解,以帮助弥合在受损的高维功能网络中如何处理生物信号的理论与实验之间的鸿沟,并为放置新的诊断工具来测量认知缺陷提供帮助。

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