Reduction of Abeta accumulation in the Tg2576 animal model of Alzheimer's disease after oral administration of the phosphatidyl-inositol kinase inhibitor wortmannin. - AlzForum Alzheimer Research Paper of the Week


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Home: Papers of the Week

Annotation

	Haugabook SJ, Le T, Yager D, Zenk B, Healy BM, Eckman EA, Prada C, Younkin L, Murphy P, Pinnix I, Onstead L, Sambamurti K, Golde TE, Dickson D, Younkin SG, Eckman CB. Reduction of Abeta accumulation in the Tg2576 animal model of Alzheimer's disease after oral administration of the phosphatidyl-inositol kinase inhibitor wortmannin. FASEB J. 2001 Jan;15(1):16-18. PubMed Abstract Corresponding Author: Christopher B. Eckman

	Comments on Paper and Primary News

	Comment by: Benjamin Wolozin, ARF Advisor (Disclosure)
	Permalink
	Wortmannin is too toxic to be used as a therapeutic, but the idea of using such inhibitors is important to be aware of. View all comments by Benjamin Wolozin

	Comment by: John Hardy, ARF Advisor
	Permalink
	I recommend this paper "An interesting paper which shows yet another way of reducing plaque load... as a result of the transgenic work, there are now many hopeful avenues for the drug industry and academics to look for Alzheimer treatments." View all comments by John Hardy

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REAGENTS/MATERIAL:
H4 neuroglioma cell line (ATCC) bAPP695sw (CHO2B7) from Dr. Todd Golde (Mayo Clinic Jacksonville, FL) Wortmannin, stock concentration (Alexis Biochemicals) Ly294002, stock concentration (Alexis Biochemicals) Anti-beta-amyloid MAb, Bam-10, IgG1, Ab1-12 (Sigma) dilution 1:10,000

FUTURE DIRECTION:
Further determination of the mechanism by which wortmannin reduces Ab accumulation. Wortmannin may be acting by influencing trafficking of bAPP and/or its metabolites, resulting in a decreased secretion of the peptide.

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