Alpha-synuclein-positive structures in cases with sporadic Alzheimer's disease: morphology and its relationship to tau aggregation. - AlzForum Alzheimer Research Paper of the Week


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Home: Papers of the Week

Annotation

	Arai Y, Yamazaki M, Mori O, Muramatsu H, Asano G, Katayama Y. Alpha-synuclein-positive structures in cases with sporadic Alzheimer's disease: morphology and its relationship to tau aggregation. Brain Res. 2001 Jan 12;888(2):287-296. PubMed Abstract Corresponding Author: Mineo Yamazaki

	Comments on Paper and Primary News

	Comment by: Benjamin Wolozin, ARF Advisor (Disclosure)
	Permalink
	I recommend this paper "Our understanding of a-synuclein pathology is limited and increasing daily. This suggests further subdivisions within AD." View all comments by Benjamin Wolozin

	Comments on Related Papers

	Related Paper: Mutation in the alpha-synuclein gene and sporadic Parkinson's disease, Alzheimer's disease, and dementia with lewy bodies. Comment by: Paul Coleman, ARF Advisor
	Permalink
	'Exploration of the ... mutation of the alpha-synuclein gene as that in familial PD (Ala53Thr) ... in sporadic PD, DLB, and AD revealed the mutation in none of the samples of 329 cases and 230 controls examined, suggesting that this mutation is not involved in these neurological diseases.' View all comments by Paul Coleman

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REAGENTS/MATERIAL:
Tissue sampling and staining anti-phosphorylated tau mAb AT8 (Innogenetic, dilution of 1:3000) anti-human beta-amyloid mAb 6F/3D (Dako, dilution of 1:100) rabbit anti-ubiquitin antibody (Dako, dilution of 1:100) Quantitation and Distribution of SPs and NFTs Neocortical SPs were identified by Bodian staining, NFTs and NTs were evaluated and classified based on Braak and Braak staging of neurofibrillary changes of AD. IH analysis LB509 mAb, raised against purified LBs specifically from DLB brains, recognizes aa 115-122, dilution of 1:50 #17 polyclonal Ab, raised against a synthetic peptide corresponding to aa 1-10 of human alpha-synuclein, dilution of 1:1000

FUTURE DIRECTION:
Study the ineraction between tau and alpha-synuclein to determine the mechanism of non-LB-type alpha-synuclein aggregation. Study the whether LB formation influence the degree of tau aggregation.

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