Alzheimer's disease is the most common brain disease which has huge social and economical burdens for the modern society. It is caused by accumulation of the toxic peptides, called amyloid beta, in the brain. There is no treatment for this devastated condition. We have identified a fragment of antibody specifically recognizing amyloid beta peptides which dissolves and remove the plaques from the brain. This project is to further test this novel drug in mouse model of the disease.
Targeting Beta-adrenergic Signalling To Improve Muscle Regeneration In Muscular Dystrophy
Funder
National Health and Medical Research Council
Funding Amount
$473,224.00
Summary
Duchenne muscular dystrophy (DMD) is the most common and severe form of muscular dystrophy, caused by a lack of a protein called dystrophin. Dystrophic muscles are fragile, prone to injury, and have a compromised ability to regenerate after damage. Modulating pathways regulating beta-adrenergic signalling has potential to attenuate the dystrophic pathology and to delay the onset or slow the progression of the muscle wasting and weakness in muscular dystrophy.