Effect of anesthetics on microglial activation and nanoparticle uptake: Implications for drug delivery in traumatic brain injury

2017 ◽  
Vol 263 ◽  
pp. 192-199 ◽  
Author(s):  
Gokul Kannan ◽  
Siva P. Kambhampati ◽  
Sapna R. Kudchadkar
Keyword(s):  
Drug Delivery ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Microglial Activation ◽  
Nanoparticle Uptake

scholarly journals Effects of Veliparib on Microglial Activation and Functional Outcomes after Traumatic Brain Injury in the Rat and Pig

2018 ◽  
Vol 35 (7) ◽  
pp. 918-929 ◽  
Author(s):  
Karen-Amanda Irvine ◽  
Robin K. Bishop ◽  
Seok Joon Won ◽  
Jianguo Xu ◽  
Katherine A. Hamel ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcomes ◽  
Microglial Activation

scholarly journals Microglia: A Potential Drug Target for Traumatic Axonal Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xin Huang ◽  
Wendong You ◽  
Yuanrun Zhu ◽  
Kangli Xu ◽  
Xiaofeng Yang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Drug Target ◽  
Microglial Activation ◽  
Axonal Injury ◽  
Traumatic Axonal Injury ◽  
Potential Drug Target ◽  
Potential Drug ◽  
Microglial Phenotype ◽  
M2 Phenotype

Traumatic axonal injury (TAI) is a major cause of death and disability among patients with severe traumatic brain injury (TBI); however, no effective therapies have been developed to treat this disorder. Neuroinflammation accompanying microglial activation after TBI is likely to be an important factor in TAI. In this review, we summarize the current research in this field, and recent studies suggest that microglial activation plays an important role in TAI development. We discuss several drugs and therapies that may aid TAI recovery by modulating the microglial phenotype following TBI. Based on the findings of recent studies, we conclude that the promotion of active microglia to the M2 phenotype is a potential drug target for the treatment of TAI.

Widespread microglial activation in patients deceased from traumatic brain injury

Brain Injury ◽  
2015 ◽  
Vol 29 (9) ◽  
pp. 1126-1133 ◽  
Author(s):  
Antonio Velázquez ◽  
Marisa Ortega ◽  
Santiago Rojas ◽  
Francisco Javier González-Oliván ◽  
Alfonso Rodríguez-Baeza
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Microglial Activation

scholarly journals Sustained Tau Phosphorylation and Microglial Activation Following Repetitive Traumatic Brain Injury

2020 ◽  
Vol 8 (A) ◽  
pp. 837-840
Author(s):  
Andre Marolop Pangihutan Siahaan ◽  
Rr Suzy Indharty ◽  
Jessy Chrestella ◽  
Wismaji Sadewo ◽  
Steven Tandean ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Treatment Group ◽  
Microglial Activation ◽  
Control Group ◽  
Sprague Dawley ◽  
Sham Control ◽  
Treatment Groups ◽  
Sham Control Group ◽  
Cd 68

BACKGROUND: Repetitive traumatic brain injury (TBI), even without acute sequela, can induce a delayed neurodegenerative with overexpression of phosphorylated tau (p-tau) as hallmark, caused by chronic inflammation mediated in part by microglial activation. AIM: The aim of this study was to examine the dynamics of p-tau accumulation and microglial activation following repetitive TBI. MATERIALS AND METHODS: Thirty Sprague–Dawley rats were randomized into a sham control group and two treatment groups receiving three successive closed-skull impacts (TBI model) from a 40-g mass dropped from a 1-m height on alternating days (days 0, 1, 3, and 7). The first treatment group was sacrificed on the last day of trauma and the second treatment group after 7 days of no trauma. The expression level of p-tau was evaluated by AT-8 antibody immunostaining and microglial activation by anti-CD-68 immunostaining. RESULTS: Immunoexpression of AT-8 was significantly elevated 7 days after TBI compared to the last day of trauma and compared to the sham control group, while CD-68 expression was significantly higher than sham controls on the last day of trauma and remained elevated for 7 days without trauma. CONCLUSION: The study showed that brain trauma can induce p-tau overexpression and microglial activation that is sustained during the non-trauma period.

scholarly journals Teriflunomide Modulates Vascular Permeability and Microglial Activation after Experimental Traumatic Brain Injury

2018 ◽  
Vol 26 (9) ◽  
pp. 2152-2162 ◽  
Author(s):  
Karthik S. Prabhakara ◽  
Daniel J. Kota ◽  
Gregory H. Jones ◽  
Amit K. Srivastava ◽  
Charles S. Cox ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Vascular Permeability ◽  
Microglial Activation ◽  
Experimental Traumatic Brain Injury

Involvement of TG-interacting factor in microglial activation during experimental traumatic brain injury

2014 ◽  
Vol 131 (6) ◽  
pp. 816-824 ◽  
Author(s):  
Chung-Ching Chio ◽  
Ching-Ping Chang ◽  
Mao-Tsun Lin ◽  
Fang-Cheng Su ◽  
Chung-Zhing Yang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Microglial Activation ◽  
Experimental Traumatic Brain Injury
Sign in / Sign up

Export Citation Format

Share Document