The complex relationship between omega-3 fatty acids and neurodegenerative diseases

by Sayuri Miyamoto

Docosahexaenoic acid (DHA) is an omega-3 fatty acid that is well known by its health-promoting effects. Being highly abundant in the brain, DHA displays essential role in neurological and visual development in infants. In adults, the decline of DHA content in brain has been associated to cognitive impairment and the use of omega-3 supplements have been thought to exert neuroprotective effects. Indeed, some studies indicated that consuming DHA would be beneficial for the prevention of cognitive disorders such as Alzheimer’s disease [1]. However, a recent clinical study involving 4000 participants has

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Together for ever…: Cross-linking of proteins by a ditryptophan bond

Cross-linking of proteins by a ditryptophan bond

by Verônica Paviani

Oxidative modifications of proteins are extensively investigated because proteins are major targets of radicals and oxidants under physiological conditions [1]. The amino acid residues most susceptible to oxidation are the sulfur-containing residues cysteine and methionine and the aromatic residues histidine, phenylalanine, tyrosine and tryptophan. The oxidation of cysteine and methionine residues is reversible and protein-cysteine oxidation is emerging as a fundamental cell regulatory mechanism. In contrast, the oxidation of all other protein residues is irreversible, and may result in loss of protein

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A novel oxidative pathway for human SOD1 aggregation is revealed and may contribute to ALS pathology

by Ohara Augusto

ALS (amyotrophic lateral sclerosis) is a fatal disease characterized by the degeneration of motor neurons, resulting in progressive muscle weakness, atrophy, paralysis and death. Most cases of ALS are sporadic but about 10% of the cases have a genetic basis.ALS-causing mutations have been identified in several genes, but the mutation of Cu,Zn superoxide dismutase gene (SOD1) is the most studied and responsible for about 20% of the familial cases. SOD1-linked ALS patients exhibit pathology and symptoms similar to those of sporadic ALS patients, leading to the hypothesis that both forms of the disease have a common pathogenic mechanism. This hypothesis led to many advances in

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