Paper
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Klunk WE, Price JC, Mathis CA, Tsopelas ND, Lopresti BJ, Ziolko SK, Bi W, Hoge JA, Cohen AD, Ikonomovic MD, Saxton JA, Snitz BE, Pollen DA, Moonis M, Lippa CF, Swearer JM, Johnson KA, Rentz DM, Fischman AJ, Aizenstein HJ, Dekosky ST. 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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This paper appears in the following:
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Comments
University of Pennsylvania
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.
Inserm
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.
Barrow Neurological Institute
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:
Klunk WE, Price JC, Mathis CA, Tsopelas ND, Lopresti BJ, Ziolko SK, Bi W, Hoge JA, Cohen AD, Ikonomovic MD, Saxton JA, Snitz BE, Pollen DA, Moonis M, Lippa CF, Swearer JM, Johnson KA, Rentz DM, Fischman AJ, Aizenstein HJ, Dekosky ST. 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.
Perez SE, Lazarov O, Koprich JB, Chen EY, Rodriguez-Menendez V, Lipton JW, Sisodia SS, Mufson EJ. Nigrostriatal dysfunction in familial Alzheimer's disease-linked APPswe/PS1DeltaE9 transgenic mice. J Neurosci. 2005 Nov 2;25(44):10220-9. PubMed.
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