IMR Press / FBL / Volume 9 / Issue 6 / DOI: 10.2741/1485

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Testing the amyloid toxicity hypothesis of Alzheimer's disease in transgenic Caenorhabditis elegans model

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1 Laboratory for Cellular and Molecular Neuroscience Research, Department of Biological Science, The University of Southern Mississippi, Hattiesburg, MS 39406, USA
Academic Editor:Yuan Luo
Front. Biosci. (Landmark Ed) 2004, 9(6), 3333–3338;
Published: 1 September 2004
(This article belongs to the Special Issue Oxidative stress, neurodegenerative disorders and neuroprotection)

Alzheimer's disease (AD) is affecting more people every year due to the increase in elderly population. This disease is characterized by senior plaques, containing aggregated amyloid beta peptide (A beta), and neurofibrillary tangles in the AD brains. The A beta depositions are thought to increase in cellular oxidative stress, which subsequently produces neuronal cell death in the patient's brain, causing loss of memory and, in the latter stages, dementia. Diverse models have been established to test this, "Amyloid Toxicity Hypothesis of AD". Among these, the use of the nematode Caenorhabditis elegans has some advantages. This invertebrate has its entire genome known, as well as numerous gene homologues to those seen in humans. In relationship with the cell model, the nematode gives the benefit of an organismal view of the disease. The nematode's short life span proves useful, when compared with that of mice, allowing mechanistic studies of the disease and pharmacological treatments. Alongside with other laboratories, we have used this in vivo model to correlate the Aβ expression with its toxicity through the observance of the organism's behavior to provide a better understanding of the cellular processes underlining AD.

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