. Beta-secretase-cleaved amyloid precursor protein accumulates at actin inclusions induced in neurons by stress or amyloid beta: a feedforward mechanism for Alzheimer's disease. J Neurosci. 2005 Dec 7;25(49):11313-21. PubMed.

Recommends

Please login to recommend the paper.

Comments

Make a Comment

To make a comment you must login or register.

Comments on this content

  1. In this paper the authors provide compelling data demonstrating that low concentrations (10 nM -1 μM) of extracellularly applied Aβ1-42 can induce rodlike inclusions in hippocampal neurons, and that similar structures are also found in brains from APP transgenic mice. Rod formation could be induced in cultured neurons by application of both fibrillar and nonfibrillar Aβ species with the latter slightly more potent than the former. Interestingly, vesicles containing APP, C99, BACE, and PS accumulate at rods. This adds to the burgeoning literature (e.g., Stokin et al., 2005; Kelly et al., 2005) that Aβ can interfere with axonal transport and cause accumulation of vesicles capable of generating additional Aβ.

    References:

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