Neurotrophin and Cannabinoids

Prevention of Alzheimer’s disease in patients with a certain genetic profile or make-up:

Alzheimer's disease is the most costly aging disease in the world, and a heavy burden to family and society. It is a progressive brain disorder that occurs gradually and results in memory loss, behavioral and personality changes, and a decline in mental abilities. These losses are related to the death of brain cells and the breakdown of the connections between them. The course of this disease varies from person to person, as does the rate of decline. People carrying Apolipoprotein E (ApoE) E4 alleles (a particular genetic mutation or genetic profile) are at high risk to develop late onset of Alzheimer’s disease. Specifically, their risk of developing Alzheimer’s disease by age 75 is 10-30 times more than other people without this genetic profile.

Based on a patented technology, funded by the NIH (National Institutes of Health), we are developing preventive medicines for people with the genes for this particular type of Alzheimer’s disease. [US20130261053 primate-specific de novo genes and cis-antisense genes, glial cell line-derived neurotrophic factor, GDNFOS.] The gene therapy uses modified small molecules, RNAi of GDNFOS and BDNFOS that are able to cross blood brain barrier and increase the neurotrophins in brain to prevent neuron death of Alzheimer’s disease, especially in the population with ApoE4 alleles.

Additionally, we are developing marijuana medicine for prevention of a particular type of Alzheimer’s disease caused by brain inflammation (US Provisional patent 62/121,227). We have generated Cnr2-floxed mice for the production of conditional mutant mouse lines to examine specific functional roles of cannabinoid receptor 2 in the brain nervous and immune systems. The Cnr2-floxed mice have been crossed with dopaminergic and microglia cell Cre-recombinase expressing mouse lines to generate conditional knockout Dat-Cnr2 and Cx3cr1-Cnr2 transgenic mice in order to study marijuana protective effects in Alzheimer's and Parkinson diseases.

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