this is exciting ....
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In animal models they have shown that production of beta-amyloid is decreased by more than 50 percent," Kaplan said. "That's the Holy Grail in terms of Alzheimer's research."
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and I am glad to hear it - but then I ran accross this and
not certain how to interpret it ...
1: Naunyn Schmiedebergs Arch Pharmacol. 2003 Sep;368(3):234-8. Epub 2003 Sep 04. Related Articles, Links
beta-Amyloid prevents excitotoxicity via recruitment of glial glutamate transporters.
Baba A, Mitsumori K, Yamada MK, Nishiyama N, Matsuki N, Ikegaya Y.
Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, 113-0033, Bunkyo-ku, Tokyo, Japan.
Amyloid beta-protein (Abeta), a putative pathogenic endotoxin involved in Alzheimer's disease, induces redistribution of glutamate transporters in astrocytes and promotes their pump activity. Because the transporters are assumed to protect neurons against excitotoxicity by removing extracellular glutamate, we hypothesized that Abeta alters the vulnerability of neurons to glutamate.
Cerebrocortical neuron-astroglial co-cultures were exposed to glutamate, the concentration of which was selected so that only 20% of the neurons exhibited degeneration.
When cultures were pre-treated with Abeta, exposure to the same "mild" glutamate concentration failed to damage neurons.
The Abeta-induced protection was abolished by a glial glutamate transporter inhibitor.
Thus, Abeta can alleviate excitotoxicity through glutamate transporter activity.
The present results may challenge prevailing concepts that Abeta-induced neuron loss causes Alzheimer's dementia and also provide practical insights into neuro-glial interactions in glutamate toxicity.
PMID: 14513203 [PubMed - in process]
ncbi.nlm.nih.gov
John McCarthy |
