Mid-Atlantic Undergraduate Research Conference – Virginia Tech
March 28, 2020
Poster Presentation
The Knockdown of HSC 70-3, Cyp1, Cnx99a, Rok, and PDGFRB and its Effect on Early Cognition in Drosophila
Alzheimer’s Disease (AD) is a neurodegenerative disorder that causes a deficit in a person’s learning and memory. This disease is caused by cell death where the tissue contains fewer nerves and connections in comparison to a “healthy brain”. When the Amyloid Precursor Protein (APP) in human brain cells are improperly cleaved, A-Beta (Aꞵ) fragments are generated which result in Aꞵ plaques. These plaques are a well-recognized marker for AD in human brains. In this work, we examined the effects of five separate APP drosophila genes through behavioral, learning, and memory assays on their larvae.
HSC 70-3, Cyp1, Cnx99a, Rok, and PDGFRB are drosophila genes with human homologs that show a strong correlation to AD. The gene HSC 70-3 plays a supportive role in the progression of tau phosphorylation (a hallmark of AD) and neurodegeneration. Cyp1 is involved with Traumatic Brain Injuries (TBIs) and cell death in neurons. Cnx99a is found in patients diagnosed with AD. In addition, the expression of Rok and a mutation in PDGFRB may be implicated in AD onset; both genes cause cell death and glial scarring after TBIs, which are known to increase the risk of developing early-onset AD. By examining these two genes, we gain perspective into a possible correlation between TBIs and early-onset AD. Using genes identified in both our lab’s RNA sequencing data from a well-characterized AD model fly and RNA sequencing data from human TBI patients, we investigated if the knockdown of these genes played a role in early cognition in larvae
March 28, 2020
Poster Presentation
The Knockdown of HSC 70-3, Cyp1, Cnx99a, Rok, and PDGFRB and its Effect on Early Cognition in Drosophila
Alzheimer’s Disease (AD) is a neurodegenerative disorder that causes a deficit in a person’s learning and memory. This disease is caused by cell death where the tissue contains fewer nerves and connections in comparison to a “healthy brain”. When the Amyloid Precursor Protein (APP) in human brain cells are improperly cleaved, A-Beta (Aꞵ) fragments are generated which result in Aꞵ plaques. These plaques are a well-recognized marker for AD in human brains. In this work, we examined the effects of five separate APP drosophila genes through behavioral, learning, and memory assays on their larvae.
HSC 70-3, Cyp1, Cnx99a, Rok, and PDGFRB are drosophila genes with human homologs that show a strong correlation to AD. The gene HSC 70-3 plays a supportive role in the progression of tau phosphorylation (a hallmark of AD) and neurodegeneration. Cyp1 is involved with Traumatic Brain Injuries (TBIs) and cell death in neurons. Cnx99a is found in patients diagnosed with AD. In addition, the expression of Rok and a mutation in PDGFRB may be implicated in AD onset; both genes cause cell death and glial scarring after TBIs, which are known to increase the risk of developing early-onset AD. By examining these two genes, we gain perspective into a possible correlation between TBIs and early-onset AD. Using genes identified in both our lab’s RNA sequencing data from a well-characterized AD model fly and RNA sequencing data from human TBI patients, we investigated if the knockdown of these genes played a role in early cognition in larvae