Continual learning (CL) requires models to learn tasks sequentially, yet deep neural networks often suffer from plasticity loss and poor knowledge transfer, which can impede their long-term adaptability. Drawing high-level inspiration from global neuromodulatory mechanisms in the brain, we introduce Neuromodulation and Synchronization (NeuMoSync), a novel architecture that integrates dynamic, neuron-specific modulation into deep neural networks to enhance their adaptability and plasticity. NeuMoSync extends standard neural network architectures with learnable feature vectors for each neuron that track network-wide historical context and with a module operating at a higher level of abstraction. This module synthesizes neuron-specific signals, conditioned on both current inputs and the network's evolving state, to adaptively regulate activation dynamics and synaptic plasticity. Evaluated on diverse CL benchmarks, including memorization (Random Label CIFAR-10 and Random Label MNIST), concept drift (Shuffle CIFAR-10 and Shuffle Mini-ImageNet), class-incremental learning (Class Split ImageNet and Class Split CIFAR-100), and domain-incremental learning (Permuted MNIST), NeuMoSync demonstrates strong performance in retaining plasticity and achieves improvements in both forward and backward adaptation compared with existing methods. Ablation studies validate the necessity of each component, while analysis of the learned modulatory signals reveals interpretable coordination patterns across tasks. Our work underscores the potential of integrating global coordination mechanisms into deep learning systems to advance robust, adaptive continual learning. The code is publicly available at https://github.com/RoozbehRazavi/NeuMoSync.
Computational models of epilepsy promise patient-specific treatment design, but most optimization workflows still search for parameters that perform well on average. In neuromodulation, this is a weak target: a protocol that improves the mean response can still fail in the patient whose network is least tolerant to stimulation. We present a literature-guided minimax pipeline that couples PubMed-scale hypothesis extraction, The Virtual Brain (TVB) Epileptor simulations, and large-language-model-guided black-box optimization. The optimizer proposes either intrinsic model-control parameters or clinically interpretable external-stimulation protocols; TVB evaluates each proposal across sampled virtual patients; and the objective maximizes worst-case reward, defined as the negative variance of simulated seizure activity. In the intrinsic model-control experiment, the best archived parameter set improved worst-case reward from -0.5285 to -0.3182, a 39.8% gain over baseline. The clinical-style external-stimulation search produced a much smaller worst-case improvement (1.7%), and a 20-patient virtual cohort showed no aggregate benefit (p=0.9019), despite a 55% responder rate and a positive temporal-lobe subgroup signal. The study should be read as an in silico proof of concept for robust, literature-aware neurostimulation design, not as clinical evidence.