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The implications of this study are manifold. First, it provides neurobiological support to the notion that anti-NMDAR encephalitis and schizophrenia are linked, as both diseases may be tied to common biological mechanisms. Second, it demonstrates the power of computational modeling as a tool to provide mechanistic explanations of long-standing enigma, like the ones NMDAR hypofunction entails. Third, it sheds light on the largely unexplored, yet potentially relevant role of associative STP in the neural computations underlying working memory. Finally, it suggests that a disruption of associative STP could be a potential treatment target for both diseases as working memory deficits are common characteristics. For instance, a recent study has demonstrated that the NMDAR antagonist memantine and the cholinergic agonist donepezil restored STP in the mouse prefrontal cortex and normalized working memory in a mouse model of schizophrenia26. Altogether, our work paves the way for a mechanistic understanding of associative STP in working memory, which could guide future treatments for the two diseases.

We also simulated our data in a model of working memory with STP dynamics and found a similar pattern of behavior: a decrease in serial dependence at the expense of information decay due to STP. However, this behavior is more complex and less precise than in our model, suggesting that serial dependence is a more sensitive measure of working memory than STP. Serial dependence is also easily integrated into models of working memory and allows the evaluation of long-term memory, leaving models of STP to explain short-term memory55,56. Most importantly, our model shows that serial dependence in working memory can emerge from NMDAR-dependent changes in synaptic potentiation, and it helps to explain why such changes are experienced as cognitive symptoms of schizophrenia and anti-NMDAR encephalitis. A biophysical model of working memory provides a more complete account of cognitive symptoms than current theories that focus on symptoms as the result of functional changes in specific brain regions57,58,59. This implies that the ability to grasp such a model may have important implications for the treatment of the related disorders, and may provide new targets for therapies.

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