Gene Therapy Prevents Memory Problems in Mice With Alzheimer's Disease
Scientists at the Gladstone Institute of Neurological Disease (GIND) in San Francisco have discovered a new strategy to prevent memory deficits in a mouse model of Alzheimer's disease (AD). Both mice genetically engineered to simulate the disease and humans who have developed AD have abnormally low levels of an enzyme called EphB2 in memory centers of the brain. Increasing EphB2 levels in such mice by gene therapy completely fixed their memory problems.
Neurotransmission, is impaired by amyloid proteins, which build up to abnormally high levels in brains of AD patients and are widely thought to cause the disease. EphB2 acts as both a receptor and an enzyme and it may be involved in the memory problems of AD because it is a master regulator of neurotransmission. The investigation aimed to study the effects relationship between EphB2 and amyloid proteins. In the study, investigators used gene therapy to experimentally alter EphB2 levels in memory centers of mice. Reducing EphB2 levels in normal healthy mice disrupted neurotransmission and gave them memory problems similar to those seen in AD, indicating a correlation between the two. Results also showed that increasing EphB2 levels in neurons of mice engineered to produce high levels of human amyloid proteins in the brain prevented their neurotransmission deficits, memory problems and behavioral abnormalities, leading to the discovery that amyloid proteins directly bind to EphB2 and cause its degradation. Scientists theorize that blocking amyloid proteins from binding to EphB2 and enhancing EphB2 levels with drugs might assist in patients with AD.
This article was interesting to me because neurodegenerative diseases such as Alzheimer’s are the some of the most difficult diseases to cure. In addition, the cause and progression of AD are currently not well understood, and any steps taken to advance the investigation of such an important topic is crucial to medical research.
http://www.sciencedaily.com/releases/2010/11/101128193748.htm
Neurotransmission, is impaired by amyloid proteins, which build up to abnormally high levels in brains of AD patients and are widely thought to cause the disease. EphB2 acts as both a receptor and an enzyme and it may be involved in the memory problems of AD because it is a master regulator of neurotransmission. The investigation aimed to study the effects relationship between EphB2 and amyloid proteins. In the study, investigators used gene therapy to experimentally alter EphB2 levels in memory centers of mice. Reducing EphB2 levels in normal healthy mice disrupted neurotransmission and gave them memory problems similar to those seen in AD, indicating a correlation between the two. Results also showed that increasing EphB2 levels in neurons of mice engineered to produce high levels of human amyloid proteins in the brain prevented their neurotransmission deficits, memory problems and behavioral abnormalities, leading to the discovery that amyloid proteins directly bind to EphB2 and cause its degradation. Scientists theorize that blocking amyloid proteins from binding to EphB2 and enhancing EphB2 levels with drugs might assist in patients with AD.
This article was interesting to me because neurodegenerative diseases such as Alzheimer’s are the some of the most difficult diseases to cure. In addition, the cause and progression of AD are currently not well understood, and any steps taken to advance the investigation of such an important topic is crucial to medical research.
http://www.sciencedaily.com/releases/2010/11/101128193748.htm
posted by DanhongYang at 9:34 PM
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