Epilepsy is a chronic neurodegenerative disease, and accumulating evidence suggests its pathological progression is closely associated with peroxynitrite (ONOO − ). However, understanding the function remains challenging due to a lack of in vivo imaging probes for ONOO − determination in epileptic brains. Here, the first near‐infrared imaging probe (named ONP) is presented for tracking endogenous ONOO − in brains of kainate‐induced epileptic seizures with high sensitivity and selectivity. Using this probe, the dynamic changes of endogenous ONOO − fluxes in epileptic brains are effectively monitored with excellent temporal and spatial resolution. In vivo visualization and in situ imaging of hippocampal regions clearly reveal that a higher concentration of ONOO − in the epileptic brains associates with severe neuronal damage and epileptogenesis; curcumin administration can eliminate excessively increased ONOO − , further effectively protecting neuronal cells. Moreover, by combining high‐content analysis and ONP, a high‐throughput screening method for antiepileptic inhibitors is constructed, which provides a rapid imaging/screening approach for understanding epilepsy pathology and accelerating antiseizure therapeutic discovery.

Abnormal accumulation of amyloid-β (Aβ) has been determined to be a critical factor for the progression of Alzheimer's disease (AD), which has motivated the development of new chemical approaches for early sensing and imaging of these Aβ aggregates. Herein, we report a new near-infrared (NIR) fluorescent probe for the selective monitoring of Aβ aggregates in vivo. This novel fluorophore, named CAQ, was based on the curcumin scaffold and was designed by introducing an intramolecular rotation donor and a quinoline functional group. CAQ was an environment-sensitive fluorescent probe that can be used as a reliable chemical tool for NIR imaging of amyloid plaques in a live Caenorhabditis elegans model of AD and in 5× FAD transgenic mice of early amyloid deposition. Our observations indicate that CAQ is promising for providing comprehensive information on neurodegenerative research, thereby promoting a deeper understanding of Alzheimer's pathological processes.

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We developed an activatable molecular agent, PNF, triggered by intracellular H2S in the lysosome to release the therapeutic drug amonafide, which can escape from the lysosome into the nucleus to induce autophagy of cancer cells.

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