Dementia has cost the country over $15 billion and is expected to exceed $36.8 billion by 2025. Currently, 436,000 Australians are affected by AD, with 1.5 million involved in their care. By 2030, global dementia cases are predicted to reach 82 million, driving the AD drug market $13.7 billion. The primary symptom of AD is memory loss, due to neuron degeneration in the hippocampus, which is crucial for memory and spatial navigation. Damage in these areas leads to disorientation, confusion, and memory problems, progressing to motor difficulties and impaired decision-making. AD is caused by neuron degeneration, involving two proteins: amyloid-beta (Aβ) and tau. Aβ causes tau to become abnormal, leading to neuron death. Tau moves from the axons to dendrites, causing synapse loss and neuron death. Aβ and tau interaction, facilitated by the NMDA receptor, is key to AD development. Professor Jürgen Götz at the Clem Jones Centre for Ageing and Dementia Research has been instrumental in developing this theory.  

The goal is to understand how mitochondrial function can reduce protein aggregation and how mitochondrial dysfunction can increase it. This involves exploring the feedback mechanisms between aging, mitochondrial function, and protein aggregation. The ultimate aim is to use this knowledge to develop combination therapies for Alzheimer’s Disease (AD) that both target and clear protein aggregates and enhance resilience mechanisms.

The goal is to understand how mitochondrial function can reduce protein aggregation and how mitochondrial dysfunction can increase it. This involves exploring the feedback mechanisms between aging, mitochondrial function, and protein aggregation. The ultimate aim is to use this knowledge to develop combination therapies for Alzheimer’s Disease (AD) that both target and clear protein aggregates and enhance resilience mechanisms.