. 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. 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.