ISNVD 2/14 Conference
Meeting and greeting so many remarkable people is such an inspiration. The energy in the room has been palpable. I think there will be a lot of excellent science presented at this conference if the keynote address is any indication.
I'm posting this as the notes I took at the presentation. I apologize for abbreviations, poor sentence structure etc but I wanted to share ASAP.
Keynote speaker...Dr. Paula Grammas PhD
The Role of Blood Vessels and Inflammation in the Pathogenesis of Neurological Disorders.
Texas Alzheimer's research and care Consortium...Director
brain endothelial cells
synthetic/metabolic capabilities...brain has more vasculature than any other part of the body
the tight junctions of the bbb are very important
the brain endothelial cells are very important metabolically
endothelial cells actively regulates the neruonal micro environment
neurpathological and neuroimaging studies indicate that 1/3 AD cases are complicated by vascular problems
AD and CVD...inflammation, oxidative stress and apoE4 expression common to both AD and CVD...
endothelial cells are widely recognized as key players in development of neurologic disease
brain endothelium produces toxins in brain in AD
blood vessels in AD...?
NO can be toxic to neurons in high doses. NO is made by endothelial cells and in small amts. is fine. in AD these cells become abnormal
AD vessels an over expression of iNOS and is usually not present in endothelial cells. this iNOS is very toxic in large amounts....caused by stress and inflammation
micro vessels in AD are inflamed
something is making the endothelial cells make inflammatory proteins
Thrombin is an inflammatory protein and is found in the AD brain in the micro vessels and CSF...inflammation in the vessels has been found in AD
vascular activation and angiogenesis have been documented in the AD brain
no new blood vessels in the AD brain...what does that mean?
vascular activation as a target for AD therapeutics
animal studies are being done now...
animals have been given a Pfizer drug (Sunitinib) causing angiogenesis have improved the animals cognitive abilities
in vitro Sunitinib improves the function of the endothelium
possible trigger for vascular activation is hypoxia
a key mediator in both angiogenesis and hypoxia is Thrombin
Thrombin inhibitors improve the function of the mice
"what's good for the heart is good for the brain"
While waiting for the cure of AD take care of any causes of inflammation (ie Diabetes) with diet and exercise.
Hypoxia stimulates the endothelial cells to create a host of inflammatory messengers designed to cause angiogenesis (creation of new blood vessels). So why is there hypoxia? Is the hypoxia chronic or intermittent? These are some questions that need to be answered!
Looking forward to the first full day of learning!