P1-417: How does elimination of TNF receptor affect amyloid-β protein generation and prevent learning and memory deficits in transgenic Alzheimer's mice?

2008 ◽  
Vol 4 ◽  
pp. T341-T342
Author(s):  
Yong Shen ◽  
Ping He ◽  
Jason Zhong ◽  
Kristina Lindholm ◽  
Gina Arnold ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Amyloid Β ◽  
Memory Deficits ◽  
Amyloid Β Protein ◽  
Tnf Receptor ◽  
Β Protein ◽  
Learning And Memory Deficits

Liraglutide protects against amyloid-β protein-induced impairment of spatial learning and memory in rats

2013 ◽  
Vol 34 (2) ◽  
pp. 576-588 ◽  
Author(s):  
Wei-Na Han ◽  
Christian Hölscher ◽  
Li Yuan ◽  
Wei Yang ◽  
Xiao-Hui Wang ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Amyloid Β ◽  
Spatial Learning And Memory ◽  
Amyloid Β Protein ◽  
Β Protein

Multicomponent Training Prevents Memory Deficit Related to Amyloid-β Protein-Induced Neurotoxicity

2021 ◽  
pp. 1-12
Author(s):  
Caroline Bitencourt Soares ◽  
Leticia Rossi Daré ◽  
Karine Ramires Lima ◽  
Luiza Freitas Lopes ◽  
Alexandre Garcia dos Santos ◽  
...  
Keyword(s):  
Recognition Memory ◽  
Physical Exercise ◽  
Amyloid Β ◽  
Memory Deficits ◽  
Amyloid Β Peptide ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Cognitive Exercise ◽  
The Brain

Background: Alzheimer’s disease (AD) is characterized by the accumulation of the amyloid-β peptide in the brain, leading to early oxidative stress and neurotoxicity. It has been suggested that physical exercise could be beneficial in preventing AD, but studies with multicomponent training are scanty. Objective: Verify the effects of multicomponent exercise training to prevent deficits in recognition memory related to Aβ neurotoxicity. Methods: We subjected Wistar rats to multicomponent training (including aerobic and anaerobic physical exercise and cognitive exercise) and then infused amyloid-β peptide into their hippocampus. Results: We show that long-term multicomponent training prevents the amyloid-β-associated neurotoxicity in the hippocampus. It reduces hippocampal lipid peroxidation, restores antioxidant capacity, and increases glutathione levels, finally preventing recognition memory deficits. Conclusion: Multicomponent training avoids memory deficits related to amyloid-β neurotoxicity on an animal model.

scholarly journals Improvement of Learning and Memory Deficits With Aerobic Training and Donepezil Co-therapy in Amyloid-β beta-injected Male Rats Through the CREB and BDNF Signaling Pathway

2020 ◽  
Author(s):  
Iman Mohseni ◽  
Maghsoud Peeri ◽  
Mohammad Ali Azarbayjani
Keyword(s):  
Alzheimer Disease ◽  
Learning And Memory ◽  
Aerobic Training ◽  
Amyloid Β ◽  
Training Group ◽  
Memory Deficits ◽  
Drug Group ◽  
Male Rats ◽  
Control Group ◽  
Learning And Memory Deficits

Background: Accumulation of amyloid-β (Aß) plaques, primarily in the hippocampus, leads to neuronal death and Alzheimer disease. Exercise and medications can prevent and treat neuronal diseases. This study aimed to determine the effects of aerobic training and donepezil, a medication used in Alzheimer disease, on the improvement of learning and memory deficits in Aß-injected male rats. Objectives: This study aimed to determine the effects of aerobic training and donepezil, a medication used in Alzheimer disease, on the improvement of learning and memory deficits in Aß-injected male rats.Methods: Male Rats were injected with an Aβ solution into their CA1 hippocampal region. After 20 days, the rats were treated with donepezil hydrochloride at doses of 2 mg/kg/d by gavage and following treadmill exercise for 4 weeks. Then, after 24 h, they performed the Morris water maze test for five days. Additionally, we studied the molecular factors involved in neuronal plasticity, such as Ca2+/cAMP-response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) on day 33. The animals were also evaluated histologically to determine the deposition of Aβ in the brain tissue. Results: Behavioral analysis showed that in the probe test, the latency to the platform zone significantly increased in the training group (F1,20=6.815; P<0.05) and in the drug group (F1,20=6.369; P<0.05). But there were no significant changes in the combined group compared with the control group (F1,20=3.909; P>0.05). Molecular analysis showed that CREB gene expression improved in the training group (F1,8=9893.539; P<0.01) and in the drug group (F1,8=631.958; P<0.01). But in the combined group, there were no significant changes compared with the Aβ group (F1,8=2.556; P>0.05). BDNF gene expression improved in the training group (F1,8=25.077; P<0.001), and in the drug group (F1,8=45.296; P<0.001). Also, in the combined group, this change was significant compared with the control group (F1,8=64.342; P<0.001). Histomorphometric analysis showed that the density of survived neurons was considerably increased in the combined group (P<0.01), and the drug group (P<0.05) compared to the control group Conclusion: In the present study, behavioral and biochemical analysis demonstrated that aerobic training and donepezil hydrochloride treatment for 4 weeks protect Aβ-injected male rats against memory impairment.

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