. Immunotherapy for Alzheimer disease: the promise and the problem. Arch Neurol. 2005 Oct;62(10):1506-7. PubMed.


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  1. The protection of synapses is, indeed, a vital component in the early treatment of AD. However, evidence suggests that the presence or absence of synapses is far from the whole synaptic story. We have shown that reduced expression of selected transcripts and proteins involved in trafficking of synaptic vesicles is found in postmortem AD brain even when other markers of synaptic structure may be unaffected (Yao et al., 2003). One of the gene products we found to be most reduced in AD was dynamin 1, a molecule critical in synaptic vesicle trafficking. More recently, Adriana Ferreira and her co-workers demonstrated that Aβ reduced the expression of dynamin 1 in hippocampal neurons (Kelly et al., 2005). These two papers suggest that markers of synaptic function would be a more sensitive marker of early synaptic deficits than markers related to only the presence or absence of synapses.


    . Defects in expression of genes related to synaptic vesicle trafficking in frontal cortex of Alzheimer's disease. Neurobiol Dis. 2003 Mar;12(2):97-109. PubMed.

    . Beta-amyloid-induced dynamin 1 depletion in hippocampal neurons. A potential mechanism for early cognitive decline in Alzheimer disease. J Biol Chem. 2005 Sep 9;280(36):31746-53. PubMed.

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  1. Making a Vaccine Work: Profiles, Protein Synthesis, and Synapses