. Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees. J Neurosci. 2007 Jun 6;27(23):6174-84. PubMed.

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  1. A provocative paper providing new insights into the onset of Abeta amyloidosis in FAD. It also raises intriguing questions as to whether or not FAD and sporadic AD and Down syndrome evolve in the same locations and same manner. It also raises question about we are how to understand the disconnection between striatal Abeta deposits and the lack of clinical symptoms, signficant neuron loss, and tau pathology linked to striatal accumulations of Abeta deposits.

  2. The work by Klunk and coworkers (2007) demonstrates how incomplete our understanding is of the early neuropathobiological events that occur in both FAD as well as sporadic AD. Interestingly, we recently demonstrated an age-related increase in striatal amyloid-containing plaques associated with neuritic pathology in APPswe/PS1δE9 mice (Perez et al., 2005). Whether striatal plaque pathology is a very early event compared to cortical and hippocampal pathology in these mice remains an unanswered question. If so, then this mutant may be a putative animal model for both AD and FAD as well as the investigation of early treatment strategies.

    References:

    . Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees. J Neurosci. 2007 Jun 6;27(23):6174-84. PubMed.

    . Nigrostriatal dysfunction in familial Alzheimer's disease-linked APPswe/PS1DeltaE9 transgenic mice. J Neurosci. 2005 Nov 2;25(44):10220-9. PubMed.

    View all comments by Elliott Mufson
  3. These findings suggest more a loss of function of APP/AICD than a gain of toxic function, since there is no correlation between the precise early distribution of amyloid and clinical impairment.