Mitochondria Dysfunction Induces Synapse Loss via Microglia Activation in AD Mice Model

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dc.contributor.advisorDu, Heng
dc.contributor.advisorGuo, Lan
dc.creatorRughwani, Tripta
dc.date.accessioned2019-10-13T00:25:35Z
dc.date.available2019-10-13T00:25:35Z
dc.date.created2019-05
dc.date.issued2019-05
dc.date.submittedMay 2019
dc.date.updated2019-10-13T00:25:36Z
dc.description.abstractAlzheimer’s disease (AD) is a chronic cognitive impairment disorder associated with synapse loss. The synaptic sites are enriched in mitochondria to provide energy for synaptic transmission/ neurotransmission. During a pathological condition like AD, the synapse is actively engulfed by reactive microglia. However, involvement of microglia in synaptic pruning due to mitochondrial dysfunction is still unclear. Here we outline various parameters that define microglial reactivity in AD mouse models. Overexpression of Oligomycin Sensitivity Conferring Protein (OSCP), an important component of F1 Fo ATP synthase helps restore mitochondrial function and rescue synapse loss. In addition, microglia in early AD brains engulf synapse in a complement dependent manner. C1q, the initiating protein of classical complement pathway decreases on restoration of mitochondrial function with OSCP overexpression. Together, these findings suggest that mitochondrial dysfunction induce synapse loss via microglial activation in AD.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/10735.1/6999
dc.language.isoen
dc.rights©2019 Tripta Rughwani
dc.subjectMicroglia
dc.subjectSynapse
dc.subjectMitochondrial pathology
dc.subjectAlzheimer's disease
dc.titleMitochondria Dysfunction Induces Synapse Loss via Microglia Activation in AD Mice Model
dc.typeThesis
dc.type.materialtext
thesis.degree.departmentBiology - Molecular and Cell Biology
thesis.degree.grantorThe University of Texas at Dallas
thesis.degree.levelMasters
thesis.degree.nameMS

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