Alzheimer’s Disease (AD) is a neurodegenerative disease and the leading cause of age-associated dementia. Although the mechanism underlying the pathogenesis of AD still remains elusive, a large body of evidence suggests that damaged mitochondria play a fundamental role in both neurons and microglia in the hippocampus. Our research focuses on delivering MSC therapies with a high bioenergetic cargo directly into the blood supply of the brain as well as modulating the blood-brain barrier through soundwave modulation.
Alzheimer’s disease (AD) is one of the major neurodegenerative diseases and is a leading cause of age-associated dementia. It is characterized by progressive brain damage that slowly destroys memory, diminishes learning ability and eventually makes patients unable to perform daily activities. AD is the eighth leading cause of death in the United States, affecting approximately 5.8 million people and accounting for nearly $290 billion in health care costs.
AD is characterized by brain lesions that include protein aggregates of senile plaques (composed of amyloid-beta (Aβ) peptides) and neurofibrillary tangles (composed of hyperphosphorylated tau). In addition, activation of microglia (i.e. a change in their state/polarization from a classic M1 phenotype to an activated M2 phenotype) is a universal feature of AD, and these cells surround and infiltrate senile plaques and neurofibrillary tangles. A promising strategy to delay/stop the progression of this disease is to use MSCs and their derived EVs. Indeed, parent MSCs and MSC-EVs have been shown to stimulate neuronal regeneration and inhibit pro-inflammatory M1 microglia, while concurrently facilitating their switch to
a protective/anti-inflammatory M2 phenotype. We are currently exploring these therapies and trying to optimize their efficacy by examining their source, culture conditions (i.e. 2D vs 3D), delivery and priming the target tissue with pulsed focused ultrasound (pFUS).