Z
Zhen Zhen Wang
Researcher at UCLA Medical Center
Publications - 6
Citations - 414
Zhen Zhen Wang is an academic researcher from UCLA Medical Center. The author has contributed to research in topics: Cerebral amyloid angiopathy & Cystatin C. The author has an hindex of 6, co-authored 6 publications receiving 403 citations. Previous affiliations of Zhen Zhen Wang include University of California, Los Angeles.
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Journal ArticleDOI
Brain parenchymal and microvascular amyloid in alzheimer's disease
TL;DR: Work with recently developed transgenic mice which express large amounts of beta/A4 in the central nervous system is likely to elucidate mechanisms by which the protein is selectively deposited in the brain in a parenchymal or microvascular form, and how it contributes to the pathogenesis of neurodegeneration.
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Giant cell arteritis in association with cerebral amyloid angiopathy: Immunohistochemical and molecular studies
Karl H. Anders,Zhen Zhen Wang,Mario Kornfeld,Françoise Gray,Virawudh Soontornniyomkij,L. A. Reed,Michael N. Hart,Michael Menchine,Diana Lenard Secor,Harry V. Vinters +9 more
TL;DR: The GCA seen in these cases of CAA most likely represents a foreign body response to amyloid proteins, causing secondary destruction of the vessel wall, and anti-smooth muscle actin immunohistochemistry suggests the occurrence of medial destruction by amyloids, with relative preservation of intimal cells.
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Toxicity of Dutch (E22Q) and Flemish (A21G) Mutant Amyloid β Proteins to Human Cerebral Microvessel and Aortic Smooth Muscle Cells
TL;DR: Investigation of the effects of 2 mutant E22Q- and A21G-Abeta peptides on smooth muscle cells from cerebral microvessels and aortic SMC found that greater toxicity in all parameters was induced, which may be linked to cell type-specific processing and metabolism of mutant forms of Abeta.
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Microvascular degeneration in hereditary cystatin C amyloid angiopathy of the brain.
TL;DR: The results indicate that cellular components of the vessel walls may play an important role in cystatin C deposition, as they do in β/A4 deposition in AD‐related CAA.
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Hypoxia and reoxygenation of brain microvascular smooth muscle cells in vitro: cellular responses and expression of cerebral amyloid angiopathy‐associated proteins
TL;DR: The results suggest that hypoxia and H/R‐induced APP and cystatin C upregulation appear to occur independently of the inhibition of cerebral MV‐SMC proliferation, and may represent an initiating event in the pathogenesis of amyloid angiopathy, or mediate progression of this microvascular lesion.