Ruiwang Huang

Abstract Tumour–neuron interactions and malignant synapse formation drive glioblastoma progression, recurrence and neurological dysfunction, but systemic inhibition of synaptic signalling causes unacceptable neurotoxicity. Here we defined the spatial and molecular determinants of malignant synapses by analysing intact human glioblastoma specimens, revealing enrichment of synapse-like structures and synapse-associated gene programmes at the tumour–brain interface.

1 Introduction Diabetes is a chronic metabolic disease characterized by hyperglycemia (Zheng et al., 2018), and type 2 diabetes mellitus (T2DM) characterized by insulin dysfunction accounts for the majority (about 95%) (Bruno et al., 2005; Holman et al., 2015). It is estimated that the prevalence rate of diabetes will gradually increase from 6.3% in 2019 to 10.2% in 2030, when the population will reach 578 million, becoming a serious global public health problem (Saeedi et al., 2019).

Introduction The prefrontal cortex (PFC) consists of several regions that are thought to play an important role in flexible decision-making. The dorsolateral PFC (dlPFC) is assumed to support executive functions (Jones and Graff-Radford, 2021), whereas the orbitofrontal cortex (OFC) appears to be involved in the flexible adaptation of behavior (Schoenbaum et al., 2021; Wang et al., 2023).