PET amyloid ligand [11C]PIB uptake shows predominantly striatal increase in variant Alzheimer's disease. - AlzForum Alzheimer Research Paper of the Week


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Home: Papers of the Week

Annotation

	Koivunen J, Verkkoniemi A, Aalto S, Paetau A, Ahonen JP, Viitanen M, Någren K, Rokka J, Haaparanta M, Kalimo H, Rinne JO. PET amyloid ligand [11C]PIB uptake shows predominantly striatal increase in variant Alzheimer's disease. Brain. 2008 Jul;131(Pt 7):1845-53. PubMed Abstract

	Comments on Paper and Primary News

	Comment by: Hilkka Soininen, ARF Advisor
	Submitted 6 July 2008 \| Permalink	Posted 9 July 2008
	I recommend this paper

	Comment by: George Perry (Disclosure)
	Submitted 4 August 2008 \| Permalink	Posted 5 August 2008
	I recommend this paper

	Comments on Related Papers

	Related Paper: Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees. Comment by: John Trojanowski, ARF Advisor
	Submitted 17 June 2007 \| Permalink	Posted 17 June 2007
	I recommend this paper 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. View all comments by John Trojanowski

	Related Paper: Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees. Comment by: Andre Delacourte, ARF Advisor
	Submitted 18 June 2007 \| Permalink	Posted 18 June 2007
	I recommend this paper 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. View all comments by Andre Delacourte

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REAGENTS/MATERIAL:
For immunostaining antibodies to Aβ, mouse monoclonal anti-Aβ 8-17 (6F/3D) (Novocastra, Newcastle, UK), mouse monoclonal to Ab17–24 (4G8) (Biodesign, Memphis, TN, USA) and rabbit polyclonal anti-Aβ 1-40 and anti-Aβ 1-42 (Biosource-QCB, Camarillo, CA, USA)

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