MicroRNA‐25 aggravates Aβ1‐42‐induced hippocampal neuron injury in Alzheimer's disease by downregulating KLF2 via the Nrf2 signaling pathway in a mouse model

2019 ◽  
Vol 120 (9) ◽  
pp. 15891-15905 ◽  
Author(s):  
Qiang Duan ◽  
Erwang Si
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Hippocampal Neuron ◽  
Nrf2 Signaling Pathway ◽  
Neuron Injury

scholarly journals Hippocampal Neuron Loss Exceeds Amyloid Plaque Load in a Transgenic Mouse Model of Alzheimer's Disease

2004 ◽  
Vol 164 (4) ◽  
pp. 1495-1502 ◽  
Author(s):  
Christoph Schmitz ◽  
Bart P.F. Rutten ◽  
Andrea Pielen ◽  
Stephanie Schäfer ◽  
Oliver Wirths ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Hippocampal Neuron ◽  
Amyloid Plaque ◽  
Transgenic Mouse Model ◽  
Neuron Loss ◽  
Model Of Alzheimer’S Disease ◽  
Plaque Load

PGE 2 -EP3 signaling pathway impairs hippocampal presynaptic long-term plasticity in a mouse model of Alzheimer's disease

2017 ◽  
Vol 50 ◽  
pp. 13-24 ◽  
Author(s):  
Vincent Maingret ◽  
Gaël Barthet ◽  
Séverine Deforges ◽  
Nan Jiang ◽  
Christophe Mulle ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Model Of Alzheimer’S Disease

scholarly journals miR-135a-5p mediates memory and synaptic impairments via the Rock2/Adducin1 signaling pathway in a mouse model of Alzheimer’s disease

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Kai Zheng ◽  
Fan Hu ◽  
Yang Zhou ◽  
Juan Zhang ◽  
Jie Zheng ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Hippocampal Neurons ◽  
Therapeutic Strategy ◽  
Memory Deficits ◽  
Synaptic Activity ◽  
Memory Impairments ◽  
Model Of Alzheimer’S Disease

AbstractAberrant regulation of microRNAs (miRNAs) has been implicated in the pathogenesis of Alzheimer’s disease (AD), but most abnormally expressed miRNAs found in AD are not regulated by synaptic activity. Here we report that dysfunction of miR-135a-5p/Rock2/Add1 results in memory/synaptic disorder in a mouse model of AD. miR-135a-5p levels are significantly reduced in excitatory hippocampal neurons of AD model mice. This decrease is tau dependent and mediated by Foxd3. Inhibition of miR-135a-5p leads to synaptic disorder and memory impairments. Furthermore, excess Rock2 levels caused by loss of miR-135a-5p plays an important role in the synaptic disorder of AD via phosphorylation of Ser726 on adducin 1 (Add1). Blocking the phosphorylation of Ser726 on Add1 with a membrane-permeable peptide effectively rescues the memory impairments in AD mice. Taken together, these findings demonstrate that synaptic-related miR-135a-5p mediates synaptic/memory deficits in AD via the Rock2/Add1 signaling pathway, illuminating a potential therapeutic strategy for AD.

scholarly journals Lycopene alleviates oxidative stress via the PI3K/Akt/Nrf2pathway in a cell model of Alzheimer’s disease

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9308 ◽  
Author(s):  
Yinchao Fang ◽  
Shanshan Ou ◽  
Tong Wu ◽  
Lingqi Zhou ◽  
Hai Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signaling Pathway ◽  
Cell Model ◽  
Chinese Hamster ◽  
Antiapoptotic Proteins ◽  
Model Of Alzheimer’S Disease ◽  
Nrf2 Signaling Pathway ◽  
Underlying Mechanisms

Background & Aims Oxidative stress (OS) plays an important role in neurodegenerative diseases such as Alzheimer’s disease (AD). Lycopene is a pigment with potent antioxidant and anti-tumor effects. However, its potential role in central nervous system is not well-defined. The aim of this study was to investigate the effect of lycopene on the cell model of AD and determine its underlying mechanisms. Methods M146L cell is a double-transfected (human APP gene and presenlin-1 gene) Chinese hamster ovary (CHO) cell line that overexpresses β -amyloid (Aβ) and is an ideal cell model for AD. We treated cells with lycopene, and observed the effect of lycopene on M146L cells. Results Oxidative stress and apoptosis in M146L cells were significantly higher than those in CHO cells, suggesting that Aβ induced OS and apoptosis. Lycopene alleviated OS and apoptosis, activated the PI3K/Akt/Nrf2 signaling pathway, upregulated antioxidant and antiapoptotic proteins and downregulated proapoptotic proteins. Additionally, lycopene inhibited β -secretase (BACE) activity in M146L cells. These results suggest that lycopene inhibits BACE activity and protects M146L cells from oxidative stress and apoptosis by activating the PI3K/Akt/Nrf2 pathway. Conclusion Lycopene possibly prevents Aβ-induced damage by activating the PI3K/Akt/Nrf2 signaling pathway and reducing the expression of BACE in M146L cells.

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