scholarly journals Flavan‐3‐ol Microbial Metabolites Modulate Proteolysis in Neuronal Cells Reducing Amyloid‐beta (1‐42) Levels

2021 ◽  
pp. 2100380
Author(s):  
Valentina Cecarini ◽  
Massimiliano Cuccioloni ◽  
Yadong Zheng ◽  
Laura Bonfili ◽  
Chunmei Gong ◽  
...  
2014 ◽  
Vol 5 (3) ◽  
Author(s):  
Yash Joshi ◽  
Domenico Praticò

AbstractAside from the well-known amyloid beta and tau pathologies found in Alzheimer’s disease (AD), neuroinflammation is a well-established aspect described in humans and animal models of the disease. Inflammatory perturbations are evident not only in neurons, but also in non-neuronal cells and cytokines in the AD brain. Although the amyloid hypothesis implicates amyloid beta (Aβ) as the prime initiator of the AD, brain inflammation in AD has a complex relationship between Aβ and tau. Using our work with the 5-lipoxygenase protein as an example, we suggest that at least in the case of AD, there is an interdependent and not necessarily hierarchical pathological relationship between Aβ, tau and inflammation.


2010 ◽  
Vol 6 ◽  
pp. S252-S252
Author(s):  
Lorena Perrone ◽  
Dirk Bartnik ◽  
Honoree Marzaguil ◽  
Susanne A. Funke ◽  
Paolo Gubellini ◽  
...  

Gerontology ◽  
1991 ◽  
Vol 37 (1) ◽  
pp. 24-30 ◽  
Author(s):  
T. Yamada ◽  
E. Araki ◽  
R. Izumi ◽  
I. Goto ◽  
H. Sasaki ◽  
...  

2006 ◽  
Vol 7 (1) ◽  
Author(s):  
Jon Nilsen ◽  
Shuhua Chen ◽  
Ronald W Irwin ◽  
Sean Iwamoto ◽  
Roberta Diaz Brinton

2021 ◽  
Vol 11 (5) ◽  
pp. 2219
Author(s):  
Hye Sook Park ◽  
Qi Qi Pang ◽  
Young Sil Kim ◽  
Ji Hyun Kim ◽  
Eun Ju Cho

Amyloid beta (Aβ) produced by the amyloidogenic pathway induces neurotoxicity, and its accumulation is a well-known cause of Alzheimer’s disease (AD). In this study, the protective effect of membrane-free stem cell extract (MFSCE) derived from adipose tissue against Aβ25–35-induced neurotoxicity in the neuronal cells was investigated. Treatment with MFSCE increased cell viability and decreased lactate dehydrogenase (LDH) release in a dose-dependent manner, compared with the Aβ25–35-induced group. The level of reactive oxygen species (ROS) was significantly increased in neuronal cells induced by Aβ25–35, whereas MFSCE treatment dose-dependently reduced ROS production. Treatment with MFSCE attenuated neuroinflammation and neuronal apoptosis by downregulating inducible nitric oxide synthase, cyclooxygenase-2, and B-cell lymphoma 2-associated X protein in treated SH-SY5Y cells induced by Aβ25–35. Furthermore, MFSCE significantly downregulated the expression of the amyloidogenic pathway-related proteins, such as amyloid precursor protein, β-secretase, preselin-1, and preselin-2. Therefore, this study indicated a neuroprotective effect of MFSCE against neurotoxicity induced by Aβ25–35, suggesting that it is a useful strategy for the treatment of AD.


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