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P1‐441: Increased parenchymal and vascular Aβ deposition in Alzheimer's disease transgenic mice with chronic hyperglycemia
Author(s) -
Sadowski Martin J.,
Pulyk Roman,
Poon Stephen Y.,
Pankiewicz Joanna E.,
Scholtzova Henrieta,
Quartermain David,
Wisniewski Thomas
Publication year - 2008
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2008.05.1023
Subject(s) - streptozotocin , genetically modified mouse , diabetes mellitus , medicine , parenchyma , endocrinology , saline , amyloid (mycology) , biology , pathology , transgene , biochemistry , gene
which can control aggregation transitions from monomers to oligomers and fibrils by employing various biological buffers and SDS-PAGE with Photoinduced Cross-Linking of Unmodified Proteins (PICUP) protocols. The results were, then, analyzed and compared to those obtained via electron microscopy and primary neuronal cell cytotoxicity assay. Results: These buffers are categorized into three basic structures having a scaffold such glycine, taurine, and tramiprosate, known as an inhibitor for A oligomerization. Depending on functional moieties of buffer’s N-terminus, oligomerization of A can be accelerated or inhibited. Conclusions: Our system can offer significant savings in time and cost for the study of the A oligomerization, where no high throughput assay is available, and the new buffer assay method can contribute to the advancement of basic experimental protocol for the development of AD treatments and imaging probes targeting assembled A in AD brains.