Yasuji Matsuoka, PhD
Assistant Professor of Neurology, Georgetown University
Alzheimer's disease is a neurodegenerative affliction associated with cognitive dysfunction. Currently available medications are effective but only show symptomatic benefits. Effective disease-modifying agents are needed to slow the clinical progression of Alzheimer's disease. Accumulation of amyloid beta (Abeta) and hyperphosphorylated tau are pathological hallmarks of Alzheimer's disease, and alternation of these pathological processes can be potential disease-modifying approaches.
My laboratory is aiming to develop therapeutic approaches for Alzheimer's diseases. This seminar includes following topics:
1. Deglycosylated antibodies enhanced Abeta efflux from the brain without evoking neuroinflammation. Neuroinflammation is a severe adverse event in Abeta immunization approach, and deglycosylated antibodies may be safer agents for passive immunization.
2. A tubulin-binding agent reduced tau phosphorylation and improved cognitive decline. This suggests a new class of compound for tau-based disease-modifying therapy.
3. Beta secretase inhibitor reduced brain Abeta in non-transgenic (wildtype) mice. This study confirmed that beta secretase inhibition is a promising approach in mice under more physiological condition, which may be more relevant to sporadic Alzheimer's cases.
Last Updated 2006/12/25