Soybean isoflavone ameliorates β-amyloid 1-42-induced learning and memory deficit in rats by protecting synaptic structure and function

Synapse ◽  
2013 ◽  
Vol 67 (12) ◽  
pp. 856-864 ◽  
Author(s):  
Juan Ding ◽  
Yuan-Di Xi ◽  
Dan-Di Zhang ◽  
Xia Zhao ◽  
Jin-Meng Liu ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Deficit ◽  
Structure And Function ◽  
Soybean Isoflavone ◽  
Synaptic Structure ◽  
Β Amyloid ◽  
Learning And Memory Deficit ◽  
And Function

EPA-enriched ethanolamine plasmalogen and EPA-enriched phosphatidylethanolamine enhance BDNF/TrkB/CREB signaling and inhibit neuronal apoptosis in vitro and in vivo

2020 ◽  
Vol 11 (2) ◽  
pp. 1729-1739 ◽  
Author(s):  
Hongxia Che ◽  
Lingyu Zhang ◽  
Lin Ding ◽  
Wancui Xie ◽  
Xiaoming Jiang ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Neuronal Apoptosis ◽  
Memory Deficit ◽  
Ethanolamine Plasmalogen ◽  
Learning And Memory Deficit

Our previous study showed that EPA-enriched ethanolamine plasmalogen (EPA-pPE) exerted more significant effects than EPA-enriched phosphatidylethanolamine (EPA-PE) in improving learning and memory deficit.

scholarly journals Tocotrienol improves learning and memory deficit of aged rats

2016 ◽  
Vol 58 (2) ◽  
pp. 114-121 ◽  
Author(s):  
Nozomi Kaneai ◽  
Kazumi Sumitani ◽  
Koji Fukui ◽  
Taisuke Koike ◽  
Hirokatsu Takatsu ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Deficit ◽  
Aged Rats ◽  
Learning And Memory Deficit

scholarly journals Regulation of synaptic structure and function by palmitoylated AMPA receptor binding protein

2010 ◽  
Vol 43 (4) ◽  
pp. 341-352 ◽  
Author(s):  
Charu Misra ◽  
Sophie Restituito ◽  
Jainne Ferreira ◽  
Gerald A. Rameau ◽  
Jie Fu ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Receptor Binding ◽  
Binding Protein ◽  
Structure And Function ◽  
Synaptic Structure ◽  
Ampa Receptor Binding Protein ◽  
And Function ◽  
Receptor Binding Protein

scholarly journals CZYH Alleviates β-Amyloid-Induced Cognitive Impairment and Inflammation Response via Modulation of JNK and NF-κB Pathway in Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Yuanyuan Deng ◽  
Lianzhi Ye ◽  
Cheng Yu ◽  
Caixia Yin ◽  
Jingshan Shi ◽  
...  
Keyword(s):  
Protein Expression ◽  
Learning And Memory ◽  
Neuroprotective Effect ◽  
Morris Water Maze Test ◽  
Nissl Staining ◽  
Neuroinflammatory Response ◽  
Neuron Loss ◽  
Pharmacological Mechanism ◽  
Β Amyloid ◽  
Learning And Memory Deficit

Cu-Zhi-Yi-Hao (CZYH), an empirical formula of traditional Chinese medicine (TCM), has been used for amnesia treatment in clinical practice. However, its underlying pharmacological mechanism has not been fully illuminated. The current study was designed to investigate the neuroprotective effect of CZYH on a β-amyloid 25-35- (Aβ25-35-) induced learning and memory deficit rat model. CZYH (200, 400, or 800 mg/kg), donepezil (1.0 mg/kg), or distilled water was given to Aβ25-35-stimulated animals for 17 days consecutively. The Morris water maze test revealed that CZYH (400 or 800 mg/kg) administration improved the Aβ25-35-induced cognitive impairments in rats, and Nissl staining demonstrated that CZYH mitigated the Aβ-caused neuron loss. In addition, CZYH treatment markedly inhibited the activation of microglia as evidenced by a decreased level of IBA-1 and increased YM-1/2 protein expression. The protein expression levels of TNF-α, IL-1β, and COX-2 were also repressed by CZYH. Besides, CZYH treatment alleviated Aβ-induced IκB-α degradation and NF-κB p65 phosphorylation, as well as reduced the JNK phosphorylation level. In conclusion, the present study suggests that CZYH could improve learning and memory abilities and relieve neuron loss in Aβ25-35-induced rats, at least partly through inhibition of the neuroinflammatory response via inhibiting the JNK-dependent NF-κB activation, indicating that CZYH might be a promising formula for the treatment of AD.

Consequences of Pharmacological BACE Inhibition on Synaptic Structure and Function

2018 ◽  
Vol 84 (7) ◽  
pp. 478-487 ◽  
Author(s):  
Kaichuan Zhu ◽  
Finn Peters ◽  
Severin Filser ◽  
Jochen Herms
Keyword(s):  
Structure And Function ◽  
Synaptic Structure ◽  
And Function

The effects of voluntary exercise on learning and memory deficit in Parkinson’s disease model of rats

2019 ◽  
Vol 15 (2) ◽  
pp. 399-405
Author(s):  
F. Rafie ◽  
V. Sheibani ◽  
M. Shahbazi ◽  
N. Naghdi ◽  
M. Pourranjbar ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Learning And Memory ◽  
Disease Model ◽  
Memory Deficit ◽  
Voluntary Exercise ◽  
Learning And Memory Deficit

Synaptopathy: dysfunction of synaptic function?

2010 ◽  
Vol 38 (2) ◽  
pp. 443-444 ◽  
Author(s):  
Nils Brose ◽  
Vincent O'Connor ◽  
Paul Skehel
Keyword(s):  
Animal Experimentation ◽  
Structure And Function ◽  
Synaptic Function ◽  
Cellular Systems ◽  
Brain Diseases ◽  
Psychiatric Disease ◽  
Synaptic Dysfunction ◽  
A Value ◽  
Synaptic Structure ◽  
And Function

Synaptopathy is an increasingly popular term used to define key features of neurodegenerative and psychiatric disease. It implies that disruptions in synaptic structure and function are potentially the major determinant of such brain diseases. The Synaptopathies: Dysfunction of Synaptic Function Biochemical Society Focused Meeting brought together several invited speakers, supplemented with short communications from young scientists, who addressed this possibility. The talks spanned the full gamut of approaches that brought molecular, cellular, systems and whole-animal experimentation together to address how fundamental synaptic biology was increasingly informing on dysfunction in disease. The disease and models thereof discussed included Alzheimer's disease, prions, Huntington's disease, Parkinson's disease, schizophrenia and autism. The audience were asked to reflect on whether synaptopathy, although attractive and conceptually useful, provided a significant explanation as the cause of these major diseases. The breadth of the meeting reinforced the complexity of these brain diseases, supported the significance of synaptic dysfunction in disease, but left open the issue as to whether the prime cause of these disorders could be resolved as simple synaptic dysfunction. Thus, despite revealing a value of synaptopathy, further investigation will be required to reveal its balance in the cause and effect in each of the major brain diseases.

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