AIRAP/AIRAPL Overexpression as a Potential Underlying Mechanism of Thymoquinone Modulation of Amyloid Beta Toxicity in Neuronal Cells
Mentor 1
Dr. Wail Hassan
Location
Union Wisconsin Room
Start Date
29-4-2016 1:30 PM
End Date
29-4-2016 3:30 PM
Description
Alzheimer’s is a neurodegenerative disease that affects an estimated 5.3 million Americans. Beta-amyloid plaques are found in the brains of Alzheimer’s patients and amyloid beta is thought to play a central role in Alzheimer’s pathogenesis. The gene that encodes for the production of amyloid beta is on chromosome 21, which patients with Down syndrome, aka trisomy 21, have an extra copy of. This extra gene copy leads to increased expression of amyloid beta. Down syndrome patients are known to develop Alzheimer’s early, around age 40. This may be attributed to the increase in amyloid without a parallel increase in clearing of the amyloid. Our study looks at modifying the expression of two genes, AIRAP, and AIRAPL and studying the cytotoxic effects of amyloid beta in the presence of thymoquinone (TQ) on mouse neuronal cells. AIRAP and AIRAPL help to increase degradation of proteins by the proteasome which would help to alleviate the toxicity of amyloid beta. The genes AIRAP and AIRAPL are human homologues of the AIP-1 gene in the Caenorhaboitis elegans worm. Upregulation of the AIP-1 gene in C. elegans has been shown to protect against amyloid beta toxicity. Expression of AIRAPL in C. elegans was able to suppress amyloid beta toxicity. Expression of AIRAP in C. elegans was not shown to alleviate toxicity. TQ is a substance that is extracted from plants and has been shown to protect neurons against amyloid beta-induced neurotoxicity in rats. We have also been able to demonstrate the alleviation of amyloid beta toxicity by TQ treatment. This research aims to define the molecular mechanisms underlying the protection offered by TQ treatment.
AIRAP/AIRAPL Overexpression as a Potential Underlying Mechanism of Thymoquinone Modulation of Amyloid Beta Toxicity in Neuronal Cells
Union Wisconsin Room
Alzheimer’s is a neurodegenerative disease that affects an estimated 5.3 million Americans. Beta-amyloid plaques are found in the brains of Alzheimer’s patients and amyloid beta is thought to play a central role in Alzheimer’s pathogenesis. The gene that encodes for the production of amyloid beta is on chromosome 21, which patients with Down syndrome, aka trisomy 21, have an extra copy of. This extra gene copy leads to increased expression of amyloid beta. Down syndrome patients are known to develop Alzheimer’s early, around age 40. This may be attributed to the increase in amyloid without a parallel increase in clearing of the amyloid. Our study looks at modifying the expression of two genes, AIRAP, and AIRAPL and studying the cytotoxic effects of amyloid beta in the presence of thymoquinone (TQ) on mouse neuronal cells. AIRAP and AIRAPL help to increase degradation of proteins by the proteasome which would help to alleviate the toxicity of amyloid beta. The genes AIRAP and AIRAPL are human homologues of the AIP-1 gene in the Caenorhaboitis elegans worm. Upregulation of the AIP-1 gene in C. elegans has been shown to protect against amyloid beta toxicity. Expression of AIRAPL in C. elegans was able to suppress amyloid beta toxicity. Expression of AIRAP in C. elegans was not shown to alleviate toxicity. TQ is a substance that is extracted from plants and has been shown to protect neurons against amyloid beta-induced neurotoxicity in rats. We have also been able to demonstrate the alleviation of amyloid beta toxicity by TQ treatment. This research aims to define the molecular mechanisms underlying the protection offered by TQ treatment.
