Publication Detail

The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.

Potent neuroprotective properties against the Alzheimer beta-amyloid by an endogenous melatonin-related indole structure, indole-3-propionic acid.

Y J Chyan; B Poeggeler; R A Omar; D G Chain; B Frangione; J Ghiso; M A Pappolla (Profiled Author: Frangione, Blas)

Departments of Pathology and Neurology, University of South Alabama, Mobile, Alabama 36617, USA.
The Journal of biological chemistry 1999;274(31):21937-42.

Widespread cerebral deposition of a 40-43-amino acid peptide called the amyloid beta-protein (Abeta) in the form of amyloid fibrils is one of the most prominent neuropathologic features of Alzheimer's disease. Numerous studies suggest that Abeta is toxic to neurons by free radical-mediated mechanisms. We have previously reported that melatonin prevents oxidative stress and death of neurons exposed to Abeta. In the process of screening indole compounds for neuroprotection against Abeta, potent neuroprotective properties were uncovered for an endogenous related species, indole-3-propionic acid (IPA). This compound has previously been identified in the plasma and cerebrospinal fluid of humans, but its functions are not known. IPA completely protected primary neurons and neuroblastoma cells against oxidative damage and death caused by exposure to Abeta, by inhibition of superoxide dismutase, or by treatment with hydrogen peroxide. In kinetic competition experiments using free radical-trapping agents, the capacity of IPA to scavenge hydroxyl radicals exceeded that of melatonin, an indoleamine considered to be the most potent naturally occurring scavenger of free radicals. In contrast with other antioxidants, IPA was not converted to reactive intermediates with pro-oxidant activity. These findings may have therapeutic applications in a broad range of clinical situations.

2 Originating Grant

• 1.

  Frangione, Blas

  Amyloidosis and Alzheimer's Disease

  1 July 1985 - 30 June 2007

  NATIONAL INSTITUTE ON AGING

  Total Funding: $ 4,467,436

• 2.

  FRANGIONE, BLAS

  AMYLOIDOSIS AND ALZHEIMERS DISEASE

  1 July 1985 - 30 June 1997

  NATIONAL INSTITUTE ON AGING

  Total Funding: $ 3,049,140

Scientific Context

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