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In severe traumatic brain injury (sTBI), acute oxidative stress and inflammatory cascades rapidly spread to cause irreversible brain damage and low survival rate within minutes. Therefore, developing a feasible solution for the quick‐treatment of life‐threatening emergency is urgently demanded to earn time for hospital treatment. Herein, Janus catalysis‐driven nanomotors (JCNs) are carefully constructed via plasma‐induced alloying technology and sputtering‐caused half‐coating strategy. The theoretical calculation and experiment results indicate that the heteroatom‐doping alloyed engine endows JCNs with much higher catalytic activity for removing reactive oxygen species and reactive nitrogen species than common Pt‐based engines. When JCNs are dropped to the surface of the ruptured skull, they can effectively catalyze endogenous hydrogen peroxide, which induces movement as fuels to promote JCNs to deep brain lesions for further nanocatalyst‐mediated cascade‐blocking therapy. The results demonstrate that the JCNs successfully block the inflammatory cascades, thereby reversing multiple behavioral defects and dramatically declining the mortality of sTBI mice. This work provides a revolutionary nanomotor‐based strategy to sense brain injury and scavenge oxidative stress. Meanwhile, the JCNs provide a feasible strategy to adapt various first‐aid scenarios due to their self‐propelled movement combined with highly multienzyme‐like catalytic activity, exhibiting tremendous therapeutic potential to help people for emergency pretreatment.

No abstract

Neurotoxic β-amyloid (Aβ) deposits are generally believed as the crucial pathogenic event in Alzheimer’s disease (AD). However, current Aβ-targeting medicines show limited therapeutic efficacy due to ineffective Aβ removal and...

The early diagnosis of Parkinson's disease (PD) provides opportunities for early intervention to slow the progression of neurological degeneration in patients, particularly as the aging population increases in our society. Among a series of pathological features of PD, mitochondria abnormalities have been identified as central event that occurs at the early stage of PD. However, the method for detecting mitochondrial abnormalities‐associated early PD has not been fully developed. We herein report a specifically mitochondrial targeting probe (named TPA‐BT‐SCP) that is able to characterize mitochondria abnormalities for early diagnosis of PD and monitor PD neurodegenerative progress. The probe is an aggregation‐induced emission (AIE) probe with a strong positive charge, a 3D distorted molecular structure, and a separated HOMO‐LUMO distribution, designed with unique molecular design guidelines. Our research demonstrated that TPA‐BT‐SCP could emit stable and strong fluorescence, and rapidly accumulate in mitochondria due to the negative charge. After intranasal administration of 1‐methy‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐induced PD mice, TPA‐BT‐SCP successfully bypassed the blood−brain barrier to light up the brain, allowing the grading of PD severity based on its high sensitivity. Taken together, this work develops a novel AIE probe that exhibits dramatically high sensitivity to mitochondrial changes and enables noninvasive diagnosis of early PD in the brain.