P4-042: The Role of Oxidative Stress and Autophagy in Amyloid Beta-protein Toxicity to Cultured Neuroblastoma Cells

2010 ◽  
Vol 6 ◽  
pp. e32-e32
Author(s):  
Lin Zheng ◽  
Nodi Dehvari ◽  
Eirikur Benedikz ◽  
Richard Cowburn ◽  
Alexei Terman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyloid Beta ◽  
Neuroblastoma Cells ◽  
Amyloid Beta Protein ◽  
Protein Toxicity

Autophagy of amyloid beta-protein in differentiated neuroblastoma cells exposed to oxidative stress

2006 ◽  
Vol 394 (3) ◽  
pp. 184-189 ◽  
Author(s):  
Lin Zheng ◽  
Karin Roberg ◽  
Fredrik Jerhammar ◽  
Jan Marcusson ◽  
Alexei Terman
Keyword(s):  
Oxidative Stress ◽  
Amyloid Beta ◽  
Neuroblastoma Cells ◽  
Amyloid Beta Protein

Role of the mitochondrial Ca2+ uniporter in Pb2+-induced oxidative stress in human neuroblastoma cells

2014 ◽  
Vol 1575 ◽  
pp. 12-21 ◽  
Author(s):  
Xinyi Yang ◽  
Bin Wang ◽  
Hongqiang Zeng ◽  
Chunqing Cai ◽  
Qiansheng Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

scholarly journals Manganese Induces Oxidative Stress, Redox State Unbalance and Disrupts Membrane Bound ATPases on Murine Neuroblastoma Cells In Vitro: Protective Role of Silymarin

2011 ◽  
Vol 36 (8) ◽  
pp. 1546-1557 ◽  
Author(s):  
Yassine Chtourou ◽  
Khaled Trabelsi ◽  
Hamadi Fetoui ◽  
Ghada Mkannez ◽  
Héla Kallel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox State ◽  
Neuroblastoma Cells ◽  
Protective Role ◽  
Murine Neuroblastoma ◽  
Membrane Bound

Compensatory mechanisms to heal neuroplasticity impairment under Alzheiemer's disease neurodegeneration. I: The role of amyloid beta and its' precursor protein

2012 ◽  
Vol 58 (4) ◽  
pp. 385-399 ◽  
Author(s):  
N.V. Koudinova ◽  
A.R. Koudinov ◽  
E.V. Kezlya ◽  
K.M. Kozirev ◽  
A.E. Medvedev ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Disease Stage ◽  
Amyloid Beta Protein ◽  
Stress Reactions ◽  
Compensatory Mechanisms ◽  
Neuronal Membranes ◽  
Normal Physiological Condition

In-depth scholar literature analysis of Alzheimer's disease neurodegenerative features of amyloid beta protein neurochemistry modification and excessive phosphorylation of tau protein (and associated neuronal cytoskeleton rearrangements) are secondary phenomena. At early disease stage these neurobiochemical mechanisms are reversible and serve to heal an impairment of biophysical properties of neuronal membranes, neurotransmission, basic neuronal function and neuroplasticity, while preserving anatomical and functional brain fields. Aβ and tau could well serve to biochemically restore physico-chemical properties of neual membranes due to a role these proteins play in lipid metabolism. Under such scenario therapeutic block of aggregation and plaque formation of Aβ and inhibition of tau phosphorylation, as well as pharmaceutical modification of other secondary neurodegenerative features (such as a cascade of oxidative stress reactions) are unable to provide an effective cure of Alzheimer's disease and related pathologies of the Central and peripheral nervous systems, because they are not arraying primary pathagenetic cause. We review the role of Aβ in compensatory mechanisms of neuroplasticity restoration under normal physiological condition and Alzheimer's disease.

Neuroprotective role of BNIP3 under oxidative stress through autophagy in neuroblastoma cells

2014 ◽  
Vol 41 (9) ◽  
pp. 5729-5734 ◽  
Author(s):  
M. Umer Farooq Awan ◽  
Murtaza Hasan ◽  
Javed Iqbal ◽  
Runhong Lei ◽  
Wang Fu Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroblastoma Cells

scholarly journals The Role of Di-Tyrosine Bonding in Amyloid Beta-Protein Assembly

2013 ◽  
Vol 104 (2) ◽  
pp. 391a ◽  
Author(s):  
Dillion Fox ◽  
Brigita Urbanc
Keyword(s):  
Amyloid Beta ◽  
Protein Assembly ◽  
Amyloid Beta Protein
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