Author response for "GAPT regulates cholinergic dysfunction and oxidative stress in the brains of learning and memory impairment mice induced by scopolamine"

Author(s):  
Zhenhong Liu ◽  
Gaofeng Qin ◽  
Lulu Mana ◽  
Yunfang Dong ◽  
Shuaiyang Huang ◽  
...  
2020 ◽  
Vol 10 (5) ◽  
Author(s):  
Zhenhong Liu ◽  
Gaofeng Qin ◽  
Lulu Mana ◽  
Yunfang Dong ◽  
Shuaiyang Huang ◽  
...  

Author(s):  
Harquin Simplice Foyet ◽  
Hervé Hervé Ngatanko Abaïssou ◽  
Eglantine Wado ◽  
Emmanuel Asongalem Acha ◽  
Ciobica Alin

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Supaporn Muchimapura ◽  
Wipawee Thukham-Mee ◽  
Kornkanok Ingkaninan ◽  
Sakchai Wittaya-Areekul

To date, the effective preventive paradigm against mild cognitive impairment (MCI) is required. Therefore, we aimed to determine whetherMangifera indicafruit extract, a substance possessing antioxidant and cognitive enhancing effects, could improve memory impairment, cholinergic dysfunction, and oxidative stress damage in animal model of mild cognitive impairment. Male Wistar rats, weighing 180–200 g, were orally given the extract at doses of 12.5, 50, and 200 mg·kg−1BW for 2 weeks before and 1 week after the bilateral injection of AF64A (icv). At the end of study, spatial memory, cholinergic neurons density, MDA level, and the activities of SOD, CAT, and GSH-Px enzymes in hippocampus were determined. The results showed that all doses of extract could improve memory together with the decreased MDA level and the increased SOD and GSH-Px enzymes activities. The increased cholinergic neurons density in CA1 and CA3 of hippocampus was also observed in rats treated with the extract at doses of 50 and 200 mg·kg−1BW. Therefore, our results suggested thatM. indica, the potential protective agent against MCI, increased cholinergic function and the decreased oxidative stress which in turn enhanced memory. However, further researches are essential to elucidate the possible active ingredients and detail mechanism.


2019 ◽  
Vol 10 (6) ◽  
pp. 3650-3659 ◽  
Author(s):  
Ji Hyun Kim ◽  
Mei Tong He ◽  
Min Jo Kim ◽  
Chang Yeol Yang ◽  
Yu Su Shin ◽  
...  

Safflower seed extract containing serotonin and its derivatives improves scopolamine-induced memory impairment, it could be a promising herbal medicine for the treatment of dementia.


2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Weixing Zhao ◽  
Zhipeng Xu ◽  
Jiangbei Cao ◽  
Qiang Fu ◽  
Yishuang Wu ◽  
...  

Abstract Background It is widely accepted that mitochondria have a direct impact on neuronal function and survival. Oxidative stress caused by mitochondrial abnormalities play an important role in the pathophysiology of lipopolysaccharide (LPS)-induced memory impairment. Elamipretide (SS-31) is a novel mitochondrion-targeted antioxidant. However, the impact of elamipretide on the cognitive sequelae of inflammatory and oxidative stress is unknown. Methods We utilized MWM and contextual fear conditioning test to assess hippocampus-related learning and memory performance. Molecular biology techniques and ELISA were used to examine mitochondrial function, oxidative stress, and the inflammatory response. TUNEL and Golgi-staining was used to detect neural cell apoptosis and the density of dendritic spines in the mouse hippocampus. Results Mice treated with LPS exhibited mitochondrial dysfunction, oxidative stress, an inflammatory response, neural cell apoptosis, and loss of dendritic spines in the hippocampus, leading to impaired hippocampus-related learning and memory performance in the MWM and contextual fear conditioning test. Treatment with elamipretide significantly ameliorated LPS-induced learning and memory impairment during behavioral tests. Notably, elamipretide not only provided protective effects against mitochondrial dysfunction and oxidative stress but also facilitated the regulation of brain-derived neurotrophic factor (BDNF) signaling, including the reversal of important synaptic-signaling proteins and increased synaptic structural complexity. Conclusion These findings indicate that LPS-induced memory impairment can be attenuated by the mitochondrion-targeted antioxidant elamipretide. Consequently, elamipretide may have a therapeutic potential in preventing damage from the oxidative stress and neuroinflammation that contribute to perioperative neurocognitive disorders (PND), which makes mitochondria a potential target for treatment strategies for PND.


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