The effects of Αβ1-40 on myosin phosphorylation in cerebrovascular smooth muscle cells
Introduction
Alzheimer's disease
• Alzheimer's disease is the most common form of dementia among the older people.
• Alzheimer's disease is one of the brain disorder, it leads to memory loss and cognitive decline.
• Alzheimer's disease is neurologically characterized by the formation of senile plaques and neurofibrillary tangles in the brain and blood vessels.
Vascular dysfunction in AD
• Αβ peptides attenuate resting CBF (K Niwa et al., 2001)
• Hemodynamic response decreased with increasing age of the animal in AD model mice (T Mueggler et al., 2003)
Ex vivo
Tissue isolation
• Basilar artery (BA) was isolated from SD rat
• Connective tissue and fat tissue were removed from vessel
• Each vessel was incubated with Amyloid peptides for up to 6h.
In vivo
Cell culture
• A10 (rat embryonic vascular smooth muscle cell) was cultured.
• They were incubated at 37°in 5% CO2 and O2 balance with amyloid peptides.
Western blot & Calcium imaging
Histology
Immunocytochemistry
To confirm increase of myosin phosphorylation-induced by amyloid beta in A-10 cells, ICC will carried out with confocal microscopy.
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Laboratory for Cognitive Neuroscience and NeuroImaging in Department of Bio and Brain Engineering, KAIST
tel +82 (0)42 350 4324 / yong@kaist.ac.kr
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