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Researcher Profile - Kim Green


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Home: Community: Researcher Profiles

Researcher Profile

RESEARCHER INFORMATION
First Name:	Kim
Last Name:	Green
Title:	Assistant Professor
Advanced Degrees:	Ph.D.
Affiliation:	University of California
Department:	Department of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders
Street Address 1:	3222 Biological Sciences 3
City:	Irvine
State/Province:	CA
Zip/Postal Code:	92697-4545
Country/Territory:	U.S.A.
Phone:	(949) 824-3859
Email Address:
Disclosure: (view policy)	Member reports no financial or other potential conflicts of interest. [Last Modified: 2 September 2003]

View all comments by Kim Green

Clinical Interests:
Alzheimer Disease, Aging Process, Stroke and Trauma

Research Focus:
A-beta PP/A-beta, Molecular and Cell biology, Oxidative Stress, Electrophysiology, Animal Models, Apoptosis/Cell cycle, Signal transduction, Tau/Cytoskeleton

Work Sector(s):
University

Web Sites:
Lab:	http://neurobiology.bio.uci.edu/faculty/laferla/

Now investigating the physiological roles of the AICD and also of ABP and any joint interactions between the two.

Firstly, is ABP actually the nasty peptide in AD, and if so why is it produced and why only in old age? The fact that there are so many enzymes which regulate both the production of ABP (ADAM10, BACE, PS-1 etc.) and its degredation (IDE etc.) suggests that ABP has a normal physiological role. What is this and will the inevitable treatments which will soon become available that prevent ABP production have other detrimental effects through its absence?

Subject BACE knockout mice to stroke and altitude experiments to see how they coped/survived compared to control groups. Likewise with APP knockouts and those overexpressing ADAM10.

Clinical trials on patients to see how cerebral vasodilators affect the onset and progress of AD.

Old age leads to a reduction in brain oxygen, both through a reduced metabolism and through a reduced Cerebral Blood Flow.

ABP is produced in response to lowered oxygen levels and serves as a "hypoxic adaptation" peptide. The aged brain responds to the lowered oxygen climate by increasing production of ABP, which becomes uncontrolled and leads to AD.

Transgenic mouse models (such as the triple transgenic model) subjected to a lowered oxygen environment, either through stroke or altitude could show accelerated progression and pathology of the disease.




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