University of
Texas Health Science Center at San Antonio researchers have developed a unique
therapeutic approach which could restore learning and memory ability in those
afflicted with Alzheimer’s Disease and other neurodegenerative diseases. Abnormalities in the expression of
cAMP-response element binding protein (CREB) have been reported in Alzheimer’s
patients. The inventors have
demonstrated improved learning and memory deficits in an animal model of
Alzheimer’s Disease by restoring CREB function via brain viral delivery of
CREB-binding protein (CBP).
Background:
Neuropathology in Alzheimer’s Disease has been
characterized by the accumulation of amyloid plaques (mainly
amyloid-β peptide) and neurofibrillary tangles
(microtubule-binding protein tau); however, the molecular pathways linking
amyloid-β accumulation to cognitive decline in Alzheimer’s
Disease remain elusive. Studies
indicate that amyloid-β induced cognitive deficits may be due to alterations in
signaling transduction pathways.
The inventors formulated a novel therapeutic approach to recover
cognitive function via signal transduction improvements critical to CREB
function and unrelated to amyloid-β and tau pathology in Alzheimer’s. Cognitive improvements in both learning
and memory were observed, without changes in amyloid-β or tau pathology, and were associated with an increase
in the level of brain-derived neurotrophic factor.
Benefits & Commercial
Application:
·
New
therapeutic approach to ameliorate cognitive deficits in Alzheimer’s
Disease
·
Improves
learning and memory deficits in an animal model of Alzheimer’s
Disease
·
Alzheimer’s Disease is currently the 6th leading cause
of death; there was a 46% rise in deaths attributed to Alzheimer’s between 2000
and 2006; mortality rates are expected to continue rising as the average age of
the baby boomer generation increases
·
Currently
only 5 drugs are approved by FDA for treatment of Alzheimer’s
symptoms
·
Alzheimer’s therapy market is expected to increase from $5.4 B in
2010 to $14.3 B in 2020
Reference:
CBP gene transfer increases BDNF levels and
ameliorates learning and memory deficits in a mouse model of Alzheimer's
disease
Status: Patent
Pending; available for exclusive licensing, collaboration
Contact
Information: John
A. Fritz.
Technology Licensing Associate
(210) 562-4033 fritzja@uthscsa.edu