This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Cerebral amyloid angiopathy is a disease in which an abnormal protein, called beta-amyloid, is deposited in the walls of blood vessels in the brain. It is known that this deposition can lead to strokes caused by bleeding from the diseased blood vessels. Our theory is that this abnormal protein deposition can also make the blood vessels too stiff, which may decrease their ability to react to normal stimuli. Brain blood vessels should normally expand to accommodate more blood flow when 1) parts of the brain become more active, such as when a subject looks at a complicated visual stimulus, or 2) there is an increase in the carbon dioxide level in the body. This expansion and increased blood flow can by detected by ultrasound of the arteries (also known as transcranial doppler ultrasound). We will test our theory by using transcranial doppler ultrasound to measure the response of blood vessels to a visual stimulus and to inhaled carbon dioxide gas. Twenty subjects with a history of bleeding stroke from cerebral amyloid angiopathy will be compared to 20 healthy controls.
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