Paclitaxel may benefit Alzheimer's and Parkinson's movement disorders

Dec 27 2004

Angiotech Pharmaceuticals have announced that a preclinical study published in today's early edition of the Proceedings of the National Academy of Sciences highlights the positive effects of Paxceed on movement disorders commonly seen in diseases known as taupathies, such as Alzheimer's and Parkinson's.

Results from the study reveal that injected paclitaxel (Paxceed) appear to restore nerve function in an animal model. In the study, it was demonstrated that low (10mg/m(2)) and medium (25mg/m(2)) doses of Paxceed had two major effects: 1) improving axonal transport and 2) increasing the amounts of tubulin and microtubules, proteins and cell structures vital for nerve structure and conduction.

"We are excited as this is the first experimental evidence to support the use of paclitaxel as a novel intervention for the treatment of Alzheimer's and other neurodegenerative diseases," said William Hunter, MD, CEO of Angiotech. "We have long believed that a microtubule stabilizing agent used systemically would hold great promise in these types of diseases, and we look forward to advancing the results of these studies into humans."

Abnormal tau proteins are often seen as mechanisms that can lead to brain degeneration in Alzheimer's disease and other neurodegenerative disorders known as taupathies. In all taupathies, there are neuropathologic aggregates of paired helical filaments and/or straight filaments composed of aberrantly phosphorylated tau proteins in central nervous system neurons or glia. It has been shown that these abnormally filamentous proteins cannot perform the important functions of binding and stabilizing microtubules which often leads to a dramatic increase in neurofibrillary tangles and neuropil threads seen in Alzheimer's. Angiotech believes that systemic paclitaxel (Paxceed), a microtubule stabilizing agent, may ultimately show a therapeutic benefit to patients with Alzheimer's disease and other taupathies by offsetting the loss of normal tau function.