The Introduction of Excess Calcium and α-Synuclein Could Alter the Recruitment of Annexin A2 to Synaptic Vesicle Membranes

dc.contributor.authorCantor, Addison
dc.date.accessioned2020-09-21T15:03:07Z
dc.date.available2020-09-21T15:03:07Z
dc.date.issued2020-04
dc.descriptionHonors Thesis Spring 2020 - Embargoeden_US
dc.description.abstractParkinson’s Disease (PD) is a neurodegenerative disorder that impairs motor function after significant neuronal loss. The underlying molecular biology of the disorder is poorly understood, and for this reason there is no treatment available that targets the root cause of the disease pathology. Mutations in and overexpression of a small, membrane binding protein called α-synuclein has been linked to neuronal dysfunction and associated with PD. α-Synuclein aggregation has been shown to impair synaptic vesicle trafficking, an essential process for neurotransmission. During neurotransmission, synaptic vesicles fuse with the plasma membrane in a process called exocytosis to release their neurotransmitters and enable communication between neurons. The released neurotransmitters bind with receptors on neighboring neurons to continue to propagate the signal. After neurotransmitter release, synaptic vesicles are formed at the presynaptic membrane in a process called endocytosis and are recycled for use during another signaling event. Preliminary data suggests [...]en_US
dc.identifier.urihttp://hdl.handle.net/11416/501
dc.publisherFlorida Southern Collegeen_US
dc.subjectParkinson's diseaseen_US
dc.subjectα-Synucleinen_US
dc.subjectNeural transmissionen_US
dc.titleThe Introduction of Excess Calcium and α-Synuclein Could Alter the Recruitment of Annexin A2 to Synaptic Vesicle Membranesen_US
dc.typeThesisen_US

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