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Literature DB >> 17401529

Effect of aldehydes derived from oxidative deamination and oxidative stress on beta-amyloid aggregation; pathological implications to Alzheimer's disease.

Abstract

Formaldehyde and methylglyoxal are generated via deamination from methylamine and aminoacetone respectively catalyzed by semicarbazide-sensitive amine oxidase (SSAO). Malondialdehyde (MDA) and 4-hydroxynonenal (HNE) are end products of lipid peroxidation due to oxidative stress. These aldehydes are capable of inducing protein cross-linkage. Elevated levels of aldehydes were found in Alzheimer's disease (AD). These reactive metabolites may potentially play important roles in beta-amyloid (Abeta) aggregation related to the pathology of AD. In the present study thioflavin-T (ThT) fluorometry, an immuno-dot-blot assay and atomic force microscopy (AFM) were employed to reveal the effect of aldehydes on Abeta aggregation in vitro. The target on Abeta for interaction with formaldehyde was identified. The results support the involvement of endogenous aldehydes in amyloid deposition related to AD.

Entities: Chemical Disease Gene

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Year: 2007 PMID： 17401529 DOI： 10.1007/s00702-007-0697-5

Source DB: PubMed Journal: J Neural Transm (Vienna) ISSN： 0300-9564 Impact factor: 3.575

27 in total

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18 in total

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4. Inhibition of aminoacylase 3 protects rat brain cortex neuronal cells from the toxicity of 4-hydroxy-2-nonenal mercapturate and 4-hydroxy-2-nonenal.

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Journal: J Neural Transm (Vienna) Date: 2013-02-08 Impact factor: 3.575