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在霍普菲尔德网络模型中估计神经退行性变和创伤性脑损伤后的记忆衰退率。

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

作者信息

Weber Melanie, Maia Pedro D, Kutz J Nathan

机构信息

Department of Applied Mathematics, University of Washington, Seattle, WA, United States.

出版信息

Front Neurosci. 2017 Nov 9;11:623. doi: 10.3389/fnins.2017.00623. eCollection 2017.

Abstract

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.

摘要

神经退行性疾病和创伤性脑损伤(TBI)是人类认知功能障碍的主要原因。在神经元网络层面,它们都广泛表现出局灶性轴突肿胀(FAS),这反过来又会损害尖峰序列中编码的信息,并导致潜在的严重功能缺陷。目前,基于FAS的影响和统计数据,尚无令人满意的记忆编码神经元网络衰退的定量预测指标。这种转化方法面临的一些挑战包括我们无法通过非侵入性方法检测小规模损伤、神经元病理学的整体复杂性,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有三个:(i)扩展霍普菲尔德的联想记忆模型,以考虑FAS的影响;(ii)根据FAS统计分布和大小的生物物理观察结果校准FAS参数;(iii)系统评估不同记忆回忆任务的恶化率,作为FAS损伤的函数。我们计算了面部识别任务的恶化率,以考虑高度相关的记忆,还计算了具有霍普菲尔德网络容量极限大小的随机、不相关记忆的辨别任务的恶化率。虽然预计任何受损网络的性能都会随着损伤而下降,但我们的结果首次将记忆回忆能力与观察到的FAS统计数据联系起来。这使得对神经元网络中脑疾病不同阶段的认知衰退进行合理估计成为可能,弥合了神经退行性变和TBI后记忆回忆受损的实验观察结果。这项工作为缩小关于受损的高维功能网络中生物信号如何处理的理论与实验之间的差距提供了新的见解,并有助于提出测量认知缺陷的新诊断工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e71/5684180/063e10e3141a/fnins-11-00623-g0001.jpg

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