More evidence suggesting that AD is associated with aberrant cell cycle events (CCEs), which appears to be linked to Abeta oligomers, and blocking beta-secretase appears to diminish the CCEs.
An excellent study supporting the mitosis failure hypothesis. We have shown previously using Affymetrix gene chips that Aβ treatment and P301L tau expression in an Alzheimer disease tissue culture model act synergistically to promote aberrant cell cycle re-entry (Hoerndli et al., 2007). Together this indicates a role for both tau and Aβ in neuronal cell cycle re-entry in AD.
References:
Hoerndli FJ, Pelech S, Papassotiropoulos A, Götz J.
Abeta treatment and P301L tau expression in an Alzheimer's disease tissue culture model act synergistically to promote aberrant cell cycle re-entry.
Eur J Neurosci. 2007 Jul;26(1):60-72.
PubMed.
Comments
University of California, Irvine
More evidence suggesting that AD is associated with aberrant cell cycle events (CCEs), which appears to be linked to Abeta oligomers, and blocking beta-secretase appears to diminish the CCEs.
The University of Queensland
An excellent study supporting the mitosis failure hypothesis. We have shown previously using Affymetrix gene chips that Aβ treatment and P301L tau expression in an Alzheimer disease tissue culture model act synergistically to promote aberrant cell cycle re-entry (Hoerndli et al., 2007). Together this indicates a role for both tau and Aβ in neuronal cell cycle re-entry in AD.
References:
Hoerndli FJ, Pelech S, Papassotiropoulos A, Götz J. Abeta treatment and P301L tau expression in an Alzheimer's disease tissue culture model act synergistically to promote aberrant cell cycle re-entry. Eur J Neurosci. 2007 Jul;26(1):60-72. PubMed.
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