Article
Neurosciences
Christa C. Huber, Eduardo A. Callegari, Maria D. Paez, Svetlana Romanova, Hongmin Wang
Summary: Exosomes, a type of extracellular vesicles, can potentially be used as a therapeutic agent for Alzheimer's disease and other neurological disorders. Heat shock treatment increases the production of exosomes from neural stem cells, which exhibit better neuroprotection against oxidative stress and amyloid-beta induced neurotoxicity compared to normal exosomes.
MOLECULAR NEUROBIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Xiong Wang, Yinong Zhang, Shigang Fei, Mian Muhammad Awais, Hao Zheng, Min Feng, Jingchen Sun
Summary: The study revealed that the Heat Shock Protein 75 (TRAP1) in Bombyx mori may play a crucial role in the proliferation of Bombyx mori nucleopolyhedrovirus, with the expression levels of TRAP1 affecting the expression of the viral capsid protein.
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
(2021)
Article
Plant Sciences
Defang Ren, Yu Fu, Li Wang, Jianqin Liu, Xia Zhong, Jiyuan Yuan, Chaoli Jiang, Honglian Wang, Zhi Li
Summary: In this study, it was demonstrated that tetrandrine ameliorates Alzheimer's disease by suppressing microglia-mediated inflammation and neurotoxicity.
Article
Biochemistry & Molecular Biology
Xinrong Pei, Fangyan Hu, Zehui Hu, Feiya Luo, Xiaoling Li, Shuxia Xing, Lei Sun, Dingxin Long
Summary: This study proves that alpha-lipoic acid (LA) can stabilize the cognitive function of patients with Alzheimer's disease (AD) and inhibit the inflammatory response induced by A beta(25-35). The Wnt/beta-catenin pathway is also involved in the protective effect of LA on microglia. These findings suggest that a combination of anti-inflammatory and antioxidant substances may offer a promising approach to the treatment of AD.
Article
Biochemistry & Molecular Biology
Chunlu Zhang, Xi Chen, Ruizhu Liu, Guoqing Zhao
Summary: This study investigated the protective effects of HSP90 inhibition and the underlying regulatory mechanisms during isoflurane-induced ferroptosis. The researchers found that the HSP90 inhibitor 17 AAG could mitigate ferroptosis and preserve the activity of the crucial protein GPX4. Additionally, 17 AAG inhibited chaperone-mediated autophagy and interfered with the formation of complexes between HSP90 and Lamp-2a, further affecting isoflurane-induced ferroptosis.
NEUROCHEMICAL RESEARCH
(2023)
Review
Biochemistry & Molecular Biology
Edward S. Wickstead
Summary: Alzheimer's disease is a common neurodegenerative disorder, especially among the elderly population, with a significant impact on society and the economy. Genome-wide association studies have identified numerous genetic loci that are associated with increased risk of AD. The use of gene editing technology and hiPSCs can provide valuable insights into the role of immune-associated genetic risk variants in AD.
Article
Neurosciences
Clivia Erb, Sabrina Reinehr, Carsten Theiss, H. Burkhard Dick, Stephanie C. Joachim
Summary: Age-related diseases such as glaucoma, a leading cause of blindness, are increasing due to an aging society. A study found that heat shock protein 27 (HSP27) is associated with glaucoma, and aged mice may be more susceptible to HSP27-induced damage compared to younger mice.
FRONTIERS IN CELLULAR NEUROSCIENCE
(2023)
Article
Environmental Sciences
Huanhuan Wang, Yao Chen, Xudan Liu, Ruo Zhang, Xiaotong Wang, Qianhui Zhang, Yuting Wei, Fang Fang, Ye Yuan, Qianqian Zhou, Yinqiao Dong, Sainan Shi, Xiaojing Jiang, Xin Li
Summary: This study investigated the mechanisms of microglia activation and TNF-alpha production induced by arsenic in the nervous system. It was found that microglia-derived TNF-alpha induced necroptosis in neuronal cells, suggesting its role in arsenic-related neurotoxicity.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2022)
Article
Food Science & Technology
Shao-Shuai Bi, Hai-Tao Jin, Milton Talukder, Jing Ge, Cong Zhang, Mei-Wei Lv, Mamoon Ali Yaqoob Ismail, Jin-Long Li
Summary: The study demonstrates a potential protective effect of Nano-Se against Cd-induced cerebellar injury in chickens, enhancing the expression of heat shock factors and heat shock proteins and alleviating cerebellar cell degradation caused by Cd treatment.
FOOD AND CHEMICAL TOXICOLOGY
(2021)
Article
Environmental Sciences
Shao-Shuai Bi, Milton Talukder, Xue-Tong Sun, Mei-Wei Lv, Jing Ge, Cong Zhang, Jin-Long Li
Summary: This study assessed the neurotoxic effects of chronic cadmium (Cd) exposure on the chicken cerebellum and investigated the expression of genes related to the heat-shock response. The results showed that Cd exposure led to clinical symptoms of ataxia in the chickens, decreased the number of Purkinje cells, and induced degeneration of Purkinje cells. Cd exposure also affected the expression of heat-shock factors and proteins. These findings shed light on the toxic effects of Cd on the cerebellum and provide evidence for the health risks posed by Cd exposure.
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
(2023)
Article
Immunology
Raissa Timmerman, Ella A. Zuiderwijk-Sick, Jeffrey J. Bajramovic
Summary: TLR-induced signaling triggers inflammatory responses, and the P2Y6 receptor enhances pro-inflammatory cytokine levels, especially in microglia. Through transcriptome analysis, P2Y6 signaling amplifies pro-inflammatory responses in microglia by regulating the expression of target genes through modulation of transcription factors. Additionally, inhibition of P2Y6 signaling strongly induces heat shock protein expression. These findings shed new light on the specific pro-inflammatory role of P2Y6 signaling in neuroinflammation and may provide novel approaches to control brain inflammatory responses.
FRONTIERS IN IMMUNOLOGY
(2022)
Article
Immunology
Brigitta Dukay, Fruzsina R. Walter, Judit P. Vigh, Beata Barabasi, Petra Hajdu, Tamas Balassa, Ede Migh, Andras Kincses, Zsofia Hoyk, Titanilla Szogi, Emoke Borbely, Balint Csoboz, Peter Horvath, Livia Fulop, Botond Penke, Laszlo Vigh, Maria A. Deli, Miklos Santha, Melinda E. Toth
Summary: The study revealed that overexpression of HSPB1 can enhance the expression of inflammatory cytokines and glial cell activation in neuroinflammatory processes, without increasing neuronal apoptosis. The results suggest that HSPB1 may play a complex role in modulating ethanol-induced neuroinflammatory responses.
JOURNAL OF NEUROINFLAMMATION
(2021)
Article
Environmental Sciences
Ge Yang, Cunyi Gong, Xinyue Zheng, Fei Hu, Jie Liu, Tian Wang, Xinyue Chen, Min Li, Zhihong Zhu, Ling Zhang, Rui Li
Summary: Studies have shown that exposure to microplastics and DEHP can individually cause neurotoxicity in animals. However, it is still uncertain whether co-exposure to these substances can also induce neurotoxicity and to what extent. This study investigated the neurotoxicity and molecular mechanisms of combined exposure to DEHP and polypropylene microplastics in immature mice. The results showed that exposure to these substances caused neurotoxic effects, including cognitive deficits, hippocampal damage, oxidative stress, and decreased brain enzyme activity.
ENVIRONMENTAL POLLUTION
(2023)
Article
Chemistry, Multidisciplinary
Li-li Xu, Jia-qian Xie, Jian-jun Shen, Mei-dan Ying, Xin-zhong Chen
Summary: Sevoflurane exposure during brain development can induce neuronal apoptosis and lead to memory and cognitive deficits. This study reveals that the lncRNA Gas5 expression is increased in exosomes derived from sevoflurane-treated neurons, and this lncRNA inhibits neuronal proliferation and induces apoptosis by promoting microglial M1 polarization and the release of inflammatory cytokines. Gas5 lncRNA upregulates Foxo3 as a competitive endogenous RNA of miR-212-3p in microglial cells, activating the NF-kappa B pathway and exacerbating neurotoxicity.
ACTA PHARMACOLOGICA SINICA
(2023)
Article
Geriatrics & Gerontology
Huijuan Shu, Zhongxin Guo, Xiangren Chen, Shuya Qi, Xinxin Xiong, Shuang Xia, Qingyun Huang, Ling Lan, Jiangu Gong, Shaoming Huang, Boning Yang, Guohe Tan
Summary: The study suggests that direct intracerebral transplantation of neural stem cells can improve cognitive function in mice exposed to manganese, possibly by enhancing neurogenesis in the host brain and providing a potential cellular basis for cognitive improvement. This research underscores the potential of treating manganese exposure through NSC transplantation.