Amyloid β-Peptide Disrupts Mitochondrial Membrane Lipid and Protein Structure: Protective Role of Tauroursodeoxycholate

2001 ◽  
Vol 281 (2) ◽  
pp. 468-474 ◽  
Author(s):  
Cecília M.P. Rodrigues ◽  
Susana Solá ◽  
Maria A. Brito ◽  
Carlos D. Brondino ◽  
Dora Brites ◽  
...  
Keyword(s):  
Protein Structure ◽  
Mitochondrial Membrane ◽  
Amyloid Β ◽  
Protective Role ◽  
Membrane Lipid ◽  
Amyloid Β Peptide ◽  
Mitochondrial Membrane Lipid

scholarly journals The role of docosahexaenoic acid in mediating mitochondrial membrane lipid oxidation and apoptosis in colonocytes

2005 ◽  
Vol 26 (11) ◽  
pp. 1914-1921 ◽  
Author(s):  
Yeevoon Ng ◽  
Rola Barhoumi ◽  
Ronald B. Tjalkens ◽  
Yang-Yi Fan ◽  
Satya Kolar ◽  
...  
Keyword(s):  
Docosahexaenoic Acid ◽  
Lipid Oxidation ◽  
Mitochondrial Membrane ◽  
Membrane Lipid ◽  
Mitochondrial Membrane Lipid

scholarly journals Astrocytes and neuroinflammation in Alzheimer's disease

2014 ◽  
Vol 42 (5) ◽  
pp. 1321-1325 ◽  
Author(s):  
Emma C. Phillips ◽  
Cara L. Croft ◽  
Ksenia Kurbatskaya ◽  
Michael J. O’Neill ◽  
Michael L. Hutton ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Responses ◽  
Amyloid Β ◽  
Synaptic Dysfunction ◽  
Amyloid Β Peptide ◽  
Substantial Evidence ◽  
Models Of Disease ◽  
Opposing Effects

Increased production of amyloid β-peptide (Aβ) and altered processing of tau in Alzheimer's disease (AD) are associated with synaptic dysfunction, neuronal death and cognitive and behavioural deficits. Neuroinflammation is also a prominent feature of AD brain and considerable evidence indicates that inflammatory events play a significant role in modulating the progression of AD. The role of microglia in AD inflammation has long been acknowledged. Substantial evidence now demonstrates that astrocyte-mediated inflammatory responses also influence pathology development, synapse health and neurodegeneration in AD. Several anti-inflammatory therapies targeting astrocytes show significant benefit in models of disease, particularly with respect to tau-associated neurodegeneration. However, the effectiveness of these approaches is complex, since modulating inflammatory pathways often has opposing effects on the development of tau and amyloid pathology, and is dependent on the precise phenotype and activities of astrocytes in different cellular environments. An increased understanding of interactions between astrocytes and neurons under different conditions is required for the development of safe and effective astrocyte-based therapies for AD and related neurodegenerative diseases.

Dietary Selenium or Zinc Supplementation Restores Brain Lipid Composition and Membrane Fluidity in Protein-Undernourished Rats

2016 ◽  
Vol 38 (6) ◽  
pp. 397-406
Author(s):  
Olusegun L. Adebayo ◽  
Bamidele A. Salau ◽  
Rajat Sandhir ◽  
Gbenga A. Adenuga
Keyword(s):  
Membrane Fluidity ◽  
Lipid Composition ◽  
Zinc Supplementation ◽  
Protective Role ◽  
Membrane Lipid ◽  
Limited Information ◽  
Total Lipids ◽  
Major Focus ◽  
Membrane Lipid Composition

Studies have shown that protein undernutrition (PU) modifies the membrane lipid composition in the intestine and liver, as well as in plasma and other areas. However, there is limited information on the effect of PU on synaptosomal membrane lipid composition and fluidity and the protective role of selenium (Se) and zinc (Zn), which is a major focus of the present study. For 10 weeks, rats were fed diets containing 16% casein, which constituted the adequate protein diet, or 5% casein, representing the PU diet. The animals were supplemented with Se and Zn at a concentration of 0.15 and 227 mg L-1, respectively, in drinking water for 3 weeks. The results showed a significant increase in total lipids, glycolipids, triglycerides, cholesterol, and the cholesterol/phospholipid (Chol/PL) ratio, and a significant reduction in phospholipids and membrane fluidity. Se and Zn supplementation to PU rats, however, significantly lowered total lipids, glycolipids, triglycerides, cholesterol, and the Chol/PL ratio, while phospholipids and membrane fluidity were significantly restored. It is concluded that a perturbed lipid composition induced by PU affects the membrane structure and fluidity, which in turn influences membrane functions. The study suggests that Se and Zn supplementation might be beneficial in restoring the lipid dyshomeostasis associated with PU.

scholarly journals Nano-assembly of amyloid β peptide: role of the hairpin fold

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Sibaprasad Maity ◽  
Mohtadin Hashemi ◽  
Yuri L. Lyubchenko
Keyword(s):  
Amyloid Β ◽  
Amyloid Β Peptide

Echinacoside ameliorates the memory impairment and cholinergic deficit induced by amyloid beta peptides via the inhibition of amyloid deposition and toxicology

2017 ◽  
Vol 8 (6) ◽  
pp. 2283-2294 ◽  
Author(s):  
Young-Ji Shiao ◽  
Muh-Hwan Su ◽  
Hang-Ching Lin ◽  
Chi-Rei Wu
Keyword(s):  
Amyloid Beta ◽  
Memory Impairment ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Protective Effects ◽  
Neuronal Function ◽  
Amyloid Beta Peptides ◽  
Beta Peptides ◽  
Amyloid Cascade

This study investigates the role of the amyloid cascade and central neuronal function on the protective effects of echinacoside in amyloid β peptide 1-42 (Aβ 1-42)-treated SH-SY5Y cells and an Aβ 1-42-infused rat.

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