. Impairment of glucose and glutamate transport and induction of mitochondrial oxidative stress and dysfunction in synaptosomes by amyloid beta-peptide: role of the lipid peroxidation product 4-hydroxynonenal. J Neurochem. 1997 Jul;69(1):273-84. PubMed.


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  1. I do not have an opinion regarding the importance of this line of research for elucidating the pathophysiology of AD. A major problem with much of the current research on amyloid beta-peptide is that the concentrations used experimentally to show that it is toxic are substantially higher than the concentrations that are likelly to be present in the AD brain, especially early in the disease when the neurons are already beginning to degenerate. Researchers in this field should focus on demonstrating that concentrations of amyloid beta-peptide that are present in the brain early in the disease are toxic. If they cannot show this, then there are serious questions about the relevance of their findings to AD.

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