Mitochondrial dysfunction due to AD pathology

Updated: about 18 hours ago
Location: Mount Lawley, WESTERN AUSTRALIA
Deadline: ;

Project Outline:

Mitochondria are important targets of the AB peptide. There is mounting evidence for mitochondria-specific AB accumulation, AD-related mitochondrial dysfunction and apoptotic cell death. Though antioxidant targeted therapeutic strategies are popular, mitochondrial targeted therapeutic strategies may be more effective for neuro protection against AB toxicity. Despite the positive links between sodium butyrate and amyloid beta, the relationship between sodium butyrate and mitochondria has not been fully characterised. Understanding the mechanistic insight of sodium butyrate on mitochondria may be the first step in developing the effective therapeutic agent for Alzheimer's disease. The proposed project will directly evaluate the effect of sodium butyrate on mitochondria which has been dysfunctional due to the deposition of amyloid beta.

Research Question:
The overall purpose of this work is to identify the effect of sodium butyrate on mitochondria which has been dysfunctional due to the deposition of amyloid beta, and in doing so gain new insight into the potential suitability of this compound as therapeutic agents for AD.

Project Area: Medical Science

School / Research Centre / Institute : School of Medical and Health Sciences research

Supervisor(s): Dr Binosha Fernando

Project level: Honours, Masters

View or Apply

Similar Positions