Unknown,Transcriptomics,Genomics,Proteomics

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Expression profiling of laser-microdissected tissue from APPPS1 plaque-depositing mouse model of Alzheimer's disease


ABSTRACT: Amyloid-M-CM-^_ (AM-CM-^_) plaques are pathological hallmarks of Alzheimer disease. However, the precise neuropathological changes that occur in brain in response to amyloid deposition are largely unknown. To study the molecular mechanism(s) responsible for AM-CM-^_-mediated neuropathology, we performed a gene expression analysis on frontal neocortical brain tissue of APPPS1 mice compared to their littermate controls. 4 samples; 2 biological replicates of each condition = 2 transgenic versus 2 non-transgenic mice; no amplification of total RNA; Cy3/Cy5 dye-swap design

ORGANISM(S): Mus musculus

SUBMITTER: Wouter Van Delm 

PROVIDER: E-GEOD-15058 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Progranulin expression correlates with dense-core amyloid plaque burden in Alzheimer disease mouse models.

Pereson Sandra S   Wils Hans H   Kleinberger Gernot G   McGowan Eileen E   Vandewoestyne Mado M   Van Broeck Bianca B   Joris Geert G   Cuijt Ivy I   Deforce Dieter D   Hutton Michael M   Van Broeckhoven Christine C   Kumar-Singh Samir S  

The Journal of pathology 20091001 2


Amyloid-beta (Abeta) plaques are pathological hallmarks of Alzheimer disease (AD). In addition, innate inflammatory responses, such as those mediated by microglia, are integral to the pathogenesis of AD. Interestingly, only dense-core plaques and not diffuse plaques are associated with neuritic and inflammatory pathology in AD patients as well as in mouse AD models. However, the precise neuropathological changes that occur in the brain in response to amyloid deposition are largely unknown. To st  ...[more]

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