Surface-bound basement membrane components accelerate amyloid-β peptide nucleation in air-free wells: An in vitro model of cerebral amyloid angiopathy

2013 ◽  
Vol 1834 (8) ◽  
pp. 1624-1631 ◽  
Author(s):  
Kazuhiro Hasegawa ◽  
Daisaku Ozawa ◽  
Tadakazu Ookoshi ◽  
Hironobu Naiki
Keyword(s):  
Basement Membrane ◽  
In Vitro Model ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Amyloid Β Peptide ◽  
Cerebral Amyloid ◽  
Vitro Model ◽  
Membrane Components ◽  
Basement Membrane Components

scholarly journals ABCA7 Downregulation Modifies Cellular Cholesterol Homeostasis and Decreases Amyloid-β Peptide Efflux in an in vitro Model of the Blood-Brain Barrier

2018 ◽  
Vol 64 (4) ◽  
pp. 1195-1211 ◽  
Author(s):  
Yordenca Lamartinière ◽  
Marie-Christine Boucau ◽  
Lucie Dehouck ◽  
Markus Krohn ◽  
Jens Pahnke ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
In Vitro Model ◽  
Amyloid Β ◽  
Cholesterol Homeostasis ◽  
Brain Barrier ◽  
Amyloid Β Peptide ◽  
Cellular Cholesterol ◽  
Blood Brain ◽  
Vitro Model

scholarly journals An in Vitro Model of Immune Complex-mediated Basement Membrane Zone Separation Caused by Pemphigoid Antibodies, Leukocytes, and Complement

1982 ◽  
Vol 78 (4) ◽  
pp. 285-290 ◽  
Author(s):  
W. Ray Gammon ◽  
Carolyn C. Merritt ◽  
Daniel M. Lewis ◽  
W. Mitchell Sams ◽  
Jaime R. Carlo ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Immune Complex ◽  
In Vitro Model ◽  
Basement Membrane Zone ◽  
Vitro Model

scholarly journals Accumulation of basement membrane components in interface between gastric carcinoma cells and fibroblasts in vitro

1987 ◽  
Vol 54 (4) ◽  
pp. 699-704 ◽  
Author(s):  
M Sobue ◽  
J Takeuchi ◽  
K Tsukidate ◽  
M Toida ◽  
S Akao ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Basement Membrane ◽  
Carcinoma Cells ◽  
Membrane Components ◽  
Basement Membrane Components

scholarly journals Aβ oligomers trigger necroptosis-mediated neurodegeneration via microglia activation in Alzheimer′s disease.

2021 ◽  
Author(s):  
Natalia Salvadores ◽  
Ines Moreno ◽  
Nazareth Gamez ◽  
Gabriel Quiroz ◽  
Laura Vegas ◽  
...  
Keyword(s):  
Microglial Activation ◽  
In Vitro Model ◽  
Amyloid Β ◽  
Etiologic Agent ◽  
Neuron Death ◽  
Aβ Oligomers ◽  
Therapeutic Implications ◽  
Tnf Α ◽  
Vitro Model

Alzheimer′s disease (AD) is a major adult-onset neurodegenerative condition with no available treatment. Compelling reports point amyloid-β (Aβ) as the main etiologic agent that triggers AD. Although there is extensive evidence of a detrimental crosstalk between Aβ and microglia that contributes to neuroinflammation in AD, the exact mechanism leading to neuron death remains unknown. Using postmortem human AD brain tissue, we show that Aβ oligomers (Aβo) colocalize with the necroptosis effector pMLKL. Moreover, we found that the burden of Aβo correlates with the expression of key markers of necroptosis activation. Additionally, inhibition of necroptosis by pharmacological or genetic means, reduce neurodegeneration and memory impairment triggered by Aβo in mice. Since microglial activation is emerging as a central driver for AD pathogenesis, we then tested the contribution of microglia to the mechanism of Aβo-mediated necroptosis activation in neurons. Using an in vitro model, we show that conditioned medium from Aβo-stimulated microglia elicited necroptosis in neurons through activation of TNF-α signaling, triggering extensive neurodegeneration. Notably, necroptosis inhibition provided significant neuronal protection. Together, these findings suggest that Aβo-mediated microglia stimulation in AD contributes to necroptosis activation in neurons and neurodegeneration. As necroptosis is a druggable degenerative mechanism, our findings might have important therapeutic implications to prevent the progression of AD.

Sign in / Sign up

Export Citation Format

Share Document