突触蛋白I
粒体自噬
神经科学
生物能学
原肌球蛋白受体激酶B
突触可塑性
创伤性脑损伤
医学
神经可塑性
线粒体
心理学
生物
内科学
受体
自噬
精神科
神经营养因子
细胞凋亡
细胞生物学
生物化学
小泡
遗传学
膜
突触小泡
作者
Pavan Thapak,Gregory S. Smith,Zhe Ying,Afshin Paydar,Neil G. Harris,Fernando Gómez‐Pinilla
标识
DOI:10.1016/j.bbadis.2023.166781
摘要
Traumatic brain injury (TBI) is major neurological burden globally, and effective treatments are urgently needed. TBI is characterized by a reduction in energy metabolism and synaptic function that seems a primary cause of neuronal dysfunction. R13, a small drug and BDNF mimetic showed promising results in improving spatial memory and anxiety-like behavior after TBI. Additionally, R13 was found to counteract reductions in molecules associated with BDNF signaling (p-TrkB, p-PI3K, p-AKT), synaptic plasticity (GluR2, PSD95, Synapsin I) as well as bioenergetic components such as mitophagy (SOD, PGC-1α, PINK1, Parkin, BNIP3, and LC3) and real-time mitochondrial respiratory capacity. Behavioral and molecular changes were accompanied by adaptations in functional connectivity assessed using MRI. Results highlight the potential of R13 as a therapeutic agent for TBI and provide valuable insights into the molecular and functional changes associated with this condition.
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