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Alzheimer's Amyloid Plaque Persistence In Vivo

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: N/A
Agency Tracking Number: 2R44AG017018-02
Amount: $485,177.00
Phase: Phase II
Program: SBIR
Solicitation Topic Code: N/A
Solicitation Number: N/A
Timeline
Solicitation Year: N/A
Award Year: 2001
Award Start Date (Proposal Award Date): N/A
Award End Date (Contract End Date): N/A
Small Business Information
12026 115TH AVE NE
KIRKLAND, WA 98034
United States
DUNS: N/A
HUBZone Owned: No
Woman Owned: No
Socially and Economically Disadvantaged: No
Principal Investigator
 ALAN SNOW
 () -
Business Contact
Phone: (425) 823-0400
Email: MCCURLEY@PROTEOTECH.COM
Research Institution
N/A
Abstract

DESCRIPTION (provided by applicant): Alzheimer's disease (AD) is a degenerative
brain disorder characterized clinically by progressive loss of memory,
cognition, reasoning, judgment and emotional stability that gradually leads to
profound mental deterioration and ultimately death. AD is the leading cause of
dementia in the elderly, today affecting 4-5 million Americans, which is
expected to double in incidence in the next 25 years. AD is characterized by
the brain accumulation of insoluble fibrillar amyloid deposits containing the
beta-amyloid protein (AB), either as extracellular amyloid plaques in the brain
parenchyma or in blood vessel walls. AB amyloid formation, deposition and
persistence in brain is believed to play a central role in AD pathogenesis by
contributing to neuronal loss and memory dysfunction, and therefore has become
a central target for the development of new drugs for the treatment of AD and
related disorders. In AD, there is currently no cure or substantially effective
treatment, and the patient usually dies within 3-10 years. .

Our Phase I SBIR studies have identified the critical importance of highly
sulfated glycosaminoglycans and related macromolecules for the in vitro
induction of maltese-cross congophilic amyloid plaque-like deposits, which are
morphologically and ultrastructurally strikingly similar to those amyloid
plaques derived from AD brain. Using this technology, we have begun to develop
in vitro screening technologies and a new non-trangenic rodent model of amyloid
plaque deposition and persistence, which is being used to rapidly identify
potential anti-amyloid plaque therapeutics that target amyloid plaque a)
deposition, b) persistence and/or c) dissolution and clearance in brain. The
major objectives of this Phase II SBIR proposal are to 1) further determine the
mechanisms of action involving heparan sulfate proteoglycans/
glycosaminoglycans in the in vitro formation of amyloid plaques of Alzheimer's
and prion diseases, 2) to further develop a non-transgenic animal model of
amyloid plaque persistence in vivo, and 3) to develop new in vitro and animal
model screening assays for the identification of anti-amyloid plaque
therapeutics.

The studies described will further establish in vitro screening and
non-transgenic animal modeling technologies for the identification of new
compounds that target amyloid plaque accumulation as it pertains to AD and
prion diseases.
PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE

* Information listed above is at the time of submission. *

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