Beneficial effects and mechanisms of regular exercise on chronic traumatic encephalopathy / 中华神经医学杂志

Physical exercise can accompany with risks, such as repeated blows to the head, causing mild traumatic brain injury (mTBI), and mTBI will cause continuous cognitive, behavioral and mental problems, bring neurodegeneration and ultimately lead to chronic traumatic encephalopathy (CTE). However, this regular exercise can also be used as a neuroprotective agent against cognitive decline in the brain and affect the plasticity of the brain. Regular exercise can improve the brain learning, memory, recognition and the disease process of CTE by reducing abnormal protein accumulation, promoting neurogenesis, synapse formation, increasing synaptic plasticity and angiogenesis, improving microcirculation, anti-microinflammation and oxidative stress, and promoting mental health. This review analyzes the pathological changes and mechanism of CTE and explore the mechanism of regular exercise in improving neurological function after CTE, so as to provide new ideas for CTE rehabilitation.

Pathological mechanism and research progress of competitive sport inducing chronic traumatic encephalopathy / 中华创伤杂志

The competitive sports are beneficial to cardiovascular system and brain health. However, physical exercise is accompanied with risks. Severe trauma is possible in competitive sports that may impact on the head and body. In recent years, more interests are aroused in sports-related traumatic brain injury(TBI), especially the mild TBI(mTBI). Repetitive mTBI can cause persistent cognitive, behavioral and mental problems, leading to chronic traumatic encephalopathy(CTE) and eventually resulting in neurodegeneration. In this study, the authors summarize the pathological characteristics and mechanism of CTE induced by mTBI due to competitive exercise so as to reveal the pathogenesis of CTE and provide valuable information for early diagnosis, development of disease biomarkers and explore effective therapeutic targets.

Role of neurovascular unit dysfunction in traumatic brain injury-induced neurodegeneration / 中华神经医学杂志

The pathological process continues to evolve for a long time after acute phase of traumatic brain injury (TBI), often coupling with neurodegeneration and neurodegenerative complications. Microvascular dysfunction and blood-brain barrier (BBB) dysfunction caused by neurovascular unit (NVU) dysfunction are closely related to the pathological process of many neurodegenerative diseases. The study on the pathological mechanism of neurovascular unit dysfunction is a promising research field of TBI-related neurodegeneration, and also provides a new idea for the treatment of neurodegeneration after TBI. Therefore, this article mainly reviews these.

Mechanism and prospect of disease-associated microglia in neurodegeneration after traumatic brain injury / 中华神经医学杂志

The pathological processes of neurodegeneration and neurodegenerative changes after traumatic brain injury (TBI) are closely related to microglia. The pathophysiological functions of microglia are closely correlated to their different cell subtypes. Disease-related microglia (DAM) are a special subtype of microglia, which recently discover on the lesions of degenerative diseases of the central nervous system. DAM are identified as important cells that induce neurodegeneration. The in-depth discussion of DAM role in pathological mechanism of neurodegeneration after TBI provides new clues for understanding and treating neurodegeneration after TBI; therefore, this article focuses on the above content and summarizes the research progress of DAM and neurodegeneration after TBI.