Gene Transfer to Improve Cognitive Dysfunction in Alzheimer’s Disease

Tech ID:

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).       



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

Small Molecule
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