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High-probability grants
According to our matching algorithm, Wolff M. Kirsch is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2002 — 2006 |
Kirsch, Wolff M. |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Iron Metabolism Alterations in Alzheimer's Disease
DESCRIPTION (provided by applicant): The institution directing this Bioengineering Research Partnership is the Loma Linda University (Neurosurgery Center for Research, Training and Education, Departments of Molecular Biology and Molecular Genetics, Biochemistry, Radiology, Radiobiology, Internal Medicine, Psychiatry and Pathology). Partners include BioErgonomics, Inc., St Paul, MN and the MRI Institute for Biomedical Research, St. Louis, MO. The goal of our multidisciplinary Bioengineering Research Partnership is to define the role of altered brain iron metabolism as a risk factor for Alzheimer's Disease in the in the context of elderly MCI patients. The engineering focus of the study is: (I) defining ex vivo markers in peripheral blood cells indicating iron or amyloid perturbations and (2) the development of a new magnetic resonance imaging (MRI) technology to quantitate and differentiate brain iron. Study subjects will be 75 patients (50 years of age or older) with minimal cognitive impairment who will be followed longitudinally for a three to four year period with sequential psychometric tests, special MRI sequences, and peripheral blood cell studies. Control subjects will consist of 25 healthy age-matched individuals who will be subjected to the same tests as the MCI group. A genetically engineered mouse with an iron regulatory protein 2 "knockout" that accumulates abnormal quantities of brain iron and displays a neurodegenerative disorder will be used to validate our new technology. A search for polymorphisms in the IRP-2 gene will be part of each patient's evaluation. At four years of serial follow-up it is anticipated that about 15% of the 75 study subjects will have AD, and correlations of psychometric data, brain iron localization and quantitation, as well as immunocytochemical peripheral blood will be established using statistical consultation and autopsy information if available.
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1 |
2018 — 2021 |
Kirsch, Wolff M. |
R43Activity Code Description: To support projects, limited in time and amount, to establish the technical merit and feasibility of R&D ideas which may ultimately lead to a commercial product(s) or service(s). R44Activity Code Description: To support in - depth development of R&D ideas whose feasibility has been established in Phase I and which are likely to result in commercial products or services. SBIR Phase II are considered 'Fast-Track' and do not require National Council Review. |
Microparticle Therapy For Cerebral Amyloid Angiopathy
ABSTRACT: Cerebral Amyloid Angiopathy (CAA), a microvasculopathy in which beta-amyloid (A?) accumulates in the walls of cerebral blood vessels, is associated with vascular fragility and bleeding secondary to blood vessel wall breakdown. CAA is especially deleterious to vascular smooth muscle cells (VSMC). CAA is found in 70-90% of AD cases, increases hemorrhagic stroke risk, and is exacerbated by amyloid immunotherapy thereby compromising this promising AD therapeutic. There is no effective therapy for CAA. Despite the prevalence of CAA in AD and the fact that AD and CAA are different diseases, CAA is often overlooked in AD studies as A? has been widely presumed to be responsible for the VSMC loss in the walls of A?-laden vessels. VSMC loss in CAA occurs due to formation of the complement system's cytolytic membrane attack complex (MAC) in the tunica media of A?-laden CAA blood vessels. Based on this discovery, our goal is to develop a first-ever therapeutic for CAA based on inhibition of MAC formation which we hypothesize will prevent CAA-induced vascular fragility. We plan to target inhibition of MAC formation in the walls of A?-laden CAA blood vessels, as opposed to systemic MAC inhibition, due to the importance of MAC for immune protection against microbial infection. We propose a ?smart? nanoparticle (SNP) made of depyrogenated chitosan that selectively targets cerebrovascular A? deposits to deliver an encapsulated CD59 plasmid whose expression abrogates the formation of MAC. We have developed a technique to depyrogenate chitosan that enables internal placement since previous chitosans are contaminated with endotoxins. These contaminants interfere with plasmid transfection and gene expression. Our chitosan depyrogenation technique is based on the application of nitrogen plasma ? the same technology employed to decontaminate potential anthrax letters sent to Congress. We are asking for a two year phase I SBIR grant since six months is too short of a time to accomplish our three specific aims. These aims are: 1) To establish successful transfection of primary human cerebral vascular smooth muscle cells (HCVSMCs) with chitosan gene-containing microparticles, 2) Induce surface expression of CD59 in HCVSMCs via microparticle transfection and 3) Establish successful protection of CD59 transfected cells from MAC-initiated cell lysis.
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0.901 |