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20. Parkinsonian Drugs in China

Author

Chen, Shengdi, Zhang, Xiaojie, Gao, Yining, Le, Weidong, Nagatsu, Toshiharu, Section editor, Nakashima, Akira, Section editor, Riederer, Peter, editor, Laux, Gerd, editor, Nagatsu, Toshiharu, editor, Le, Weidong, editor, and Riederer, Christian, editor

Published
2022
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21. Anti-dementia Medications: Specific Agents

Author

Zhang, Feng, Liu, Xinyao, Liu, Yufei, Wang, Yanjiang, Le, Weidong, Vecsei, Laszlo, Section editor, Riederer, Peter, editor, Laux, Gerd, editor, Nagatsu, Toshiharu, editor, Le, Weidong, editor, and Riederer, Christian, editor

Published
2022
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28. Autophagy and Alzheimer’s Disease

Author

Chen, Sheng, Zhou, Qinming, Ni, You, Le, Weidong, Crusio, Wim E., Series Editor, Dong, Haidong, Series Editor, Radeke, Heinfried H., Series Editor, Rezaei, Nima, Series Editor, and Le, Weidong, editor

Published
2020
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29. Autophagy and Motor Neuron Diseases

Author

Zhang, Xiaojie, Yang, Kang, Le, Weidong, Crusio, Wim E., Series Editor, Dong, Haidong, Series Editor, Radeke, Heinfried H., Series Editor, Rezaei, Nima, Series Editor, and Le, Weidong, editor

Published
2020
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33. Deficiency in endocannabinoid synthase DAGLB contributes to early onset Parkinsonism and murine nigral dopaminergic neuron dysfunction

Author

Liu, Zhenhua, Yang, Nannan, Dong, Jie, Tian, Wotu, Chang, Lisa, Ma, Jinghong, Guo, Jifeng, Tan, Jieqiong, Dong, Ao, He, Kaikai, Zhou, Jingheng, Cinar, Resat, Wu, Junbing, Salinas, Armando G., Sun, Lixin, Kumar, Mantosh, Sullivan, Breanna T., Oldham, Braden B., Pitz, Vanessa, Makarious, Mary B., Ding, Jinhui, Kung, Justin, Xie, Chengsong, Hawes, Sarah L., Wang, Lupeng, Wang, Tao, Chan, Piu, Zhang, Zhuohua, Le, Weidong, Chen, Shengdi, Lovinger, David M., Blauwendraat, Cornelis, Singleton, Andrew B., Cui, Guohong, Li, Yulong, Cai, Huaibin, and Tang, Beisha

Published
2022
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37. Protein disulfide isomerase disassembles stress granules and blocks cytoplasmic aggregation of TDP-43 in ALS

Author

Liu, Jia-Qi, primary, Liu, Hao, additional, Li, Yuying, additional, Liu, Xiangyi, additional, Wang, Li-Qiang, additional, Wang, Kan, additional, Yang, Zhaofei, additional, Fu, Qi, additional, Xu, Xiaojiao, additional, Chen, Jie, additional, Zhang, Yingshuang, additional, Zhou, Jun, additional, Le, Weidong, additional, Cui, Mengchao, additional, and Liang, Yi, additional

Published
2024
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41. Fecal microbiota from patients with Parkinson's disease intensifies inflammation and neurodegeneration in A53T mice.

Author

Yang, Huijia, Shao, Yaping, Hu, Yiying, Qian, Jin, Wang, Panpan, Tian, Lulu, Ni, Yang, Li, Song, Al‐Nusaif, Murad, Liu, Cong, and Le, Weidong

Subjects
INTESTINAL barrier function, FECAL microbiota transplantation, PARKINSON'S disease, PATHOLOGICAL physiology, GUT microbiome
Abstract

Aims: We evaluated the potential of Parkinson's disease (PD) fecal microbiota transplantation to initiate or exacerbate PD pathologies and investigated the underlying mechanisms. Methods: We transplanted the fecal microbiota from PD patients into mice by oral gavage and assessed the motor and intestinal functions, as well as the inflammatory and pathological changes in the colon and brain. Furthermore, 16S rRNA gene sequencing combined with metabolomics analysis was conducted to assess the impacts of fecal delivery on the fecal microbiota and metabolism in recipient mice. Results: The fecal microbiota from PD patients increased intestinal inflammation, deteriorated intestinal barrier function, intensified microglia and astrocyte activation, abnormal deposition of α‐Synuclein, and dopaminergic neuronal loss in the brains of A53T mice. A mechanistic study revealed that the fecal microbiota of PD patients stimulated the TLR4/NF‐κB/NLRP3 pathway in both the brain and colon. Additionally, multiomics analysis found that transplantation of fecal microbiota from PD patients not only altered the composition of the gut microbiota but also influenced the fecal metabolic profile of the recipient mice. Conclusion: The fecal microbiota from PD patients intensifies inflammation and neurodegeneration in A53T mice. Our findings demonstrate that imbalance and dysfunction in the gut microbiome play significant roles in the development and advancement of PD. [ABSTRACT FROM AUTHOR]

Published
2024
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42. Cerebellum in Alzheimer's disease and other neurodegenerative diseases: an emerging research frontier.

Author

Yang, Cui, Liu, Guangdong, Chen, Xi, and Le, Weidong

Subjects
ALZHEIMER'S disease, LEWY body dementia, NEURODEGENERATION, CEREBELLUM diseases, HUNTINGTON disease, FRONTOTEMPORAL lobar degeneration
Abstract

The cerebellum is crucial for both motor and nonmotor functions. Alzheimer's disease (AD), alongside other dementias such as vascular dementia (VaD), Lewy body dementia (DLB), and frontotemporal dementia (FTD), as well as other neurodegenerative diseases (NDs) like Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and spinocerebellar ataxias (SCA), are characterized by specific and non‐specific neurodegenerations in central nervous system. Previously, the cerebellum's significance in these conditions was underestimated. However, advancing research has elevated its profile as a critical node in disease pathology. We comprehensively review the existing evidence to elucidate the relationship between cerebellum and the aforementioned diseases. Our findings reveal a growing body of research unequivocally establishing a link between the cerebellum and AD, other forms of dementia, and other NDs, supported by clinical evidence, pathological and biochemical profiles, structural and functional neuroimaging data, and electrophysiological findings. By contrasting cerebellar observations with those from the cerebral cortex and hippocampus, we highlight the cerebellum's distinct role in the disease processes. Furthermore, we also explore the emerging therapeutic potential of targeting cerebellum for the treatment of these diseases. This review underscores the importance of the cerebellum in these diseases, offering new insights into the disease mechanisms and novel therapeutic strategies. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Terahertz Irradiation Improves Cognitive Impairments and Attenuates Alzheimer's Neuropathology in the APPSWE/PS1DE9 Mouse: A Novel Therapeutic Intervention for Alzheimer's Disease.

Author

Zhang, Jun, Chen, Yixin, Zhao, Yarui, Wang, Panpan, Ding, Hongbin, Liu, Cong, Lyu, Junhong, and Le, Weidong

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the deposition of amyloid-β (Aβ), neurofibrillary tangles, neuroinflammation, and neurodegeneration in the brain. In recent years, considering the unsatisfied benefits of pharmacological therapies, non-pharmacological therapy has become a research hotspot for AD intervention. Terahertz (THz) waves with a range between microwave and infrared regions in the electromagnetic spectrum and high permeability to a wide range of materials have great potential in the bioengineering field. However, its biological impacts on the central nervous system, under either physiological or pathological conditions, are poorly investigated. In this study, we first measured the 0.14 THz waves penetration across the skull of a C57BL/6 mouse and found the percentage of THz penetration to be ~70%, guaranteeing that THz waves can reach the relevant brain regions. We then exposed the APPSWE/PS1DE9 mouse model of AD to repeated low-frequency THz waves on the head. We demonstrated that THz waves treatment significantly improved the cognitive impairment and alleviated AD neuropathology including Aβ deposition and tau hyperphosphorylation in the AD mice. Moreover, THz waves treatment effectively attenuated mitochondrial impairment, neuroinflammation, and neuronal loss in the AD mouse brain. Our findings reveal previously unappreciated beneficial effects of THz waves treatment in AD and suggest that THz waves may have the potential to be used as a novel therapeutic intervention for this devastating disease. [ABSTRACT FROM AUTHOR]

Published
2024
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