Title : Mitochondria and Alzheimer’s disease: Participation of Miro protein
Alzheimer’s disease (AD) is a neurodegenerative disease, characterized by loss of memory and cognitive impairment due to the accumulation amyloid beta 42 (Aβ42) plaque and neurofibrillary tangles (NFT) due the hyperphosphorylated Tau protein in the parts of brain. Due a significant increase in AD patent number world-wide (~50 million people worldwide), it has been considered as one of the most challenging problems that need immediate concern. Several lines of evidences suggested that mitochondria play a crucial role in the onset of several neurodegenerative diseases including AD. It has been also shown that abnormality with mitochondrial function is the first step of development of AD and related pathologies. Miro, a Rho GTPases and mitochondrial outer membrane protein forms a major protein complex with Milton, and mediates mitochondrial axonal transport. In AD, an abnormal mitochondrial function and altered axonal transport has been reported but the possible link between Miro and AD associate genes (Appl, Aβ42 and Tau) is not well understood. Herein, using Drosophila melanogaster, an invertebrate model, we have demonstrated the possible genetic interaction between Miro and Appl, Aβ42 and Tau gene in Drosophila.
What will audience learn from your presentation?
- Audience will understand about Alzheimer’s disease
- They will understand about the molecular details of AD and key players regulating the AD.
- For a teacher, the talk will be helpful to understand the mitochondrial role in AD progression and use of invertebrate model organism for AD research.