. Axonal accumulation of synaptic markers in APP transgenic Drosophila depends on the NPTY motif and is paralleled by defects in synaptic plasticity. Eur J Neurosci. 2007 Feb;25(4):1079-86. PubMed.

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  1. The interesting paper of Rusu and coworkers describes that axonal accumulation of synaptic markers in the fruit fly depends on the NPTY motif of APP. APP overexpression induced a partial but characteristic axonal transport phenotype, which correlated with deficits in short-term synaptic plasticity. This report further supports previous findings in mouse models with mutant or wild-type APP overexpression (1,2), which also elicit aberrant intraneuronal accumulation of Aβ peptides upon reduction of kinesin-I (1). This is an interesting link as intraneuronal Aβ accumulation correlates well with age-dependent axonal degeneration (3,4) and neuron loss of CA1 pyramidal cells (5,6) in two different APP/PS1 mouse lines. It would be interesting to learn whether the NPTY-dependent axonal phenotype in the fruit fly is also based on elevated (intracellular) Aβ accumulation.
      

    References:

    . Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease. Science. 2005 Feb 25;307(5713):1282-8. PubMed.

    . Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration. Neuron. 2006 Jul 6;51(1):29-42. PubMed.

    . Axonopathy in an APP/PS1 transgenic mouse model of Alzheimer's disease. Acta Neuropathol. 2006 Apr;111(4):312-9. PubMed.

    . Age-dependent axonal degeneration in an Alzheimer mouse model. Neurobiol Aging. 2007 Nov;28(11):1689-99. PubMed.

    . Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease. Am J Pathol. 2004 Apr;164(4):1495-502. PubMed.

    . Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Abeta42 accumulation in a novel Alzheimer transgenic model. Am J Pathol. 2004 Oct;165(4):1289-300. PubMed.

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