MRI-guided focused ultrasound therapy against amyloid-beta
Sunnybrook Research Institute
The pathology of Alzheimer’s disease includes the accumulation of amyloid-beta peptides in the brain, leading to the formation of amyloid plaques and rendering the brain tissue unhealthy. Amyloid-beta peptides can contribute to the deterioration of neurons, a cell type in the brain which is involved in functions such as learning and memory.
Previous therapies relied on reducing to toxicity of amyloid-beta peptides to the brain by delivering antibodies against amyloid-beta in the blood. These approaches were successful in clearing amyloid-beta peptides away from the brain but they failed to significantly protect learning and memory. We hypothesize that targeting amyloid-beta toxicity directly into the brain will be more effective.
To test this hypothesis, we will use a promising ultrasound technology, guided by magnetic resonance imaging (MRI), to deliver long-acting therapeutics from the blood to targeted areas of the brain. This will be done in a pre-clinical mouse model of Alzheimer’s disease.
Relevance to the acceleration of therapeutics for neurodegenerative diseases of aging
If successful, MRI-guided focused ultrasound therapy to the brain can be translated to the clinic for Alzheimer’s disease. In addition, MRI-guided focused ultrasound therapy can target other pathologies related to Alzheimer’s disease and age-related neurodegenerative disorders. MRI-guided focused ultrasound could fulfill a long sought-after goal of delivering therapeutics to diseased brain areas non-invasively, and resulting in lasting beneficial effects.
Non-invasive delivery of therapeutics to the brain remains a major challenge for the treatment of neurological disorders. Our research could transform current invasive methods of delivering therapeutics to the brain into non-surgical treatments. MRI-guided focused ultrasound offers a unique non-invasive approach to deliver therapeutics to the brain. It could become ‘a one-time treatment’ supplying disease-modifying agents to the brain for months, and even years. Positive outcomes of our research in terms of improving cognitive functions and reducing amyloid-beta pathology in our pre-clinical mouse model of Alzheimer’s disease would support the translation of this approach to the clinic.