The role of β-amyloid peptide in neurodegenerative diseases

2011 ◽  
Vol 10 (4) ◽  
pp. 440-452 ◽  
Author(s):  
A.V. Maltsev ◽  
S. Bystryak ◽  
O.V. Galzitskaya
Keyword(s):  
Neurodegenerative Diseases ◽  
Amyloid Peptide ◽  
Β Amyloid ◽  
Β Amyloid Peptide

4-12-07 Ischemic animals as model in the study of the neurobiological role of human β-amyloid peptide

1997 ◽  
Vol 150 ◽  
pp. S227
Author(s):  
R. Pluta ◽  
M. Barcikowska ◽  
A. Misicka ◽  
S. Januszewski ◽  
A.W. Lipkowski
Keyword(s):  
Amyloid Peptide ◽  
Β Amyloid ◽  
Β Amyloid Peptide

scholarly journals The Characterization of the Caenorhabditis elegans Mitochondrial Thioredoxin System Uncovers an Unexpected Protective Role of Thioredoxin Reductase 2 in β-Amyloid Peptide Toxicity

2012 ◽  
Vol 16 (12) ◽  
pp. 1384-1400 ◽  
Author(s):  
Briseida Cacho-Valadez ◽  
Fernando Muñoz-Lobato ◽  
José Rafael Pedrajas ◽  
Juan Cabello ◽  
Juan Carlos Fierro-González ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Thioredoxin Reductase ◽  
Protective Role ◽  
Amyloid Peptide ◽  
Thioredoxin System ◽  
Β Amyloid ◽  
Β Amyloid Peptide

Phosphorylation promotes Al(iii) binding to proteins: GEGEGSGG as a case study

2016 ◽  
Vol 18 (10) ◽  
pp. 7197-7207 ◽  
Author(s):  
Rafael Grande-Aztatzi ◽  
Elena Formoso ◽  
Jon I. Mujika ◽  
Jesus M. Ugalde ◽  
Xabier Lopez
Keyword(s):  
Neurodegenerative Diseases ◽  
Everyday Life ◽  
Amyloid Peptide ◽  
Peptide Aggregation ◽  
The Third ◽  
Β Amyloid ◽  
Abundant Element ◽  
Earth's Crust ◽  
Β Amyloid Peptide

Aluminum, the third most abundant element in the Earth's crust and one of the key industrial components of our everyday life, has been associated with several neurodegenerative diseases due to its ability to promote neurofilament tangles and β-amyloid peptide aggregation.

Protective role of N-trans-feruloyltyramine against β-amyloid peptide-induced neurotoxicity in rat cultured cortical neurons

2012 ◽  
Vol 513 (2) ◽  
pp. 229-232 ◽  
Author(s):  
Wipawan Thangnipon ◽  
Nirut Suwanna ◽  
Narisorn Kitiyanant ◽  
Rungtip Soi-ampornkul ◽  
Patoomratana Tuchinda ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Protective Role ◽  
Amyloid Peptide ◽  
Cultured Cortical Neurons ◽  
Β Amyloid ◽  
Β Amyloid Peptide

scholarly journals The Interplay between Ca2+ Signaling Pathways and Neurodegeneration

2019 ◽  
Vol 20 (23) ◽  
pp. 6004 ◽  
Author(s):  
Ureshino ◽  
Erustes ◽  
Bassani ◽  
Wachilewski ◽  
Guarache ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Temporal Organization ◽  
Amyloid Peptide ◽  
Physiological Processes ◽  
Stress Energy ◽  
The Central Nervous System ◽  
Β Amyloid Peptide ◽  
And Function ◽  
Related Proteins

Calcium (Ca2+) homeostasis is essential for cell maintenance since this ion participates in many physiological processes. For example, the spatial and temporal organization of Ca2+ signaling in the central nervous system is fundamental for neurotransmission, where local changes in cytosolic Ca2+ concentration are needed to transmit information from neuron to neuron, between neurons and glia, and even regulating local blood flow according to the required activity. However, under pathological conditions, Ca2+ homeostasis is altered, with increased cytoplasmic Ca2+ concentrations leading to the activation of proteases, lipases, and nucleases. This review aimed to highlight the role of Ca2+ signaling in neurodegenerative disease-related apoptosis, where the regulation of intracellular Ca2+ homeostasis depends on coordinated interactions between the endoplasmic reticulum, mitochondria, and lysosomes, as well as specific transport mechanisms. In neurodegenerative diseases, alterations-increased oxidative stress, energy metabolism alterations, and protein aggregation have been identified. The aggregation of α-synuclein, β-amyloid peptide (Aβ), and huntingtin all adversely affect Ca2+ homeostasis. Due to the mounting evidence for the relevance of Ca2+ signaling in neuroprotection, we would focus on the expression and function of Ca2+ signaling-related proteins, in terms of the effects on autophagy regulation and the onset and progression of neurodegenerative diseases.

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