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P4–008: Modulation of Aβ production and deposition by 12/15 lipoxygenase in vivo
Author(s) -
Pratico Domenico,
Firuzi Omidreza,
Townsend Kirk,
Chinnici Cinzia,
Wood Marcelo,
Abel Ted
Publication year - 2006
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.2006.05.1746
Subject(s) - in vivo , genetically modified mouse , pathogenesis , lipoxygenase , oxidative stress , polyunsaturated fatty acid , transgene , enzyme , chemistry , phenotype , alzheimer's disease , inflammation , in vitro , microbiology and biotechnology , disease , biochemistry , biology , endocrinology , medicine , gene , genetics , fatty acid
paraformaldehyde. On completion of the perfusion, the head of the animal was carefully removed and soaked in 4% paraformaldehyde. Fixed brain specimens were kept at 4 °C prior to the MRI study. MRI was performed on a Bruker AV 500 Wide Bore NMR spectrometer (11.7T, 500 MHz 1H frequency) with the Bruker Microimaging accessory at Bruker BioSpin Corp., USA. The data were analyzed with one-way ANOVA test. The level of significance was set at P 0.05. Both MRI of brain specimen and histological image analysis showed large and dense deposits of plaques on the lesion side, especially areas adjacent to the infarct and hippocampus. In the present study, an increase in A staining was observed in the ischemic border zone and in the hippocampus of the ischemic side. Given that the accumulation of A is associated with neurodegeneration after brain injury, acute necrotic damage and a long-lasting degenerative process are likely to contribute to the dense deposits of plaques. Ischemia caused transient accumulation of A in the ischemic border zone. Our data might provide insight into possible mechanisms related to the pathologic protein accumulation commonly observed in Alzheimer disease because it has been suggested that progression of the pathology in AD is related to the connections between the areas displaying early deposits. This finding might aid in furthering our understanding of the generation, deposition and clearance of amyloid deposits in Alzheimer disease.