Diagnosing and treating patients more effectively earlier will, even if you aren’t able to instigate a cure, offer the ability to modify the disease progression and slow or delay when brain damage occurs. In the case of Alzheimer’s, once the amyloid plaques (tangles of misshapen proteins) have accumulated in nervous tissue, it has so far been impossible to untangle or remove them.
In a letter to the science journal Nature, published online on August 21, 2011, scientists from Northwestern University in Chicago report findings that could help develop drugs for patients with Amyotrophic Lateral Sclerosis (ALS), more commonly known as Lou Gehrig’s disease.
ALS is a progressive, fatal, degenerative motor neurone disease, which results in the inability to walk, get out of bed, move arms, hands, swallow or chew. Unlike Alzheimer’s disease, cognitive functions are not usually impaired, making it a particularly nasty disease when faced with awareness of disease progression.
It’s a fact of human life that we lose physical and mental function as we get older. In the information age that we currently live in, this translates into a decline in our ability to function and perform the activities of daily living. Can we halt or delay age-related memory loss?
Due to the pressure of other commitments, I only had the pleasure of attending the annual meeting of the Association for Research in Vision and Ophthalmology (ARVO) for two days, but one of my key take home messages from the meeting is how we can use the eye as a window into the brain. This is particularly relevant to Alzheimer’s research.
ARVO researchers at a lunchtime workshop that I attended asked the question of what can we learn from shared disease mechanisms in age-related macular degeneration (AMD), Alzheimer’s Disease (AD) and Glaucoma to devise therapies of the future?
This month is Parkinson’s awareness month. Following on from my recent interview (that you can read here & here) with Dr Todd Sherer of The Michael J. Fox Foundation for Parkinson’s Research, I was interested to read about progress being made on the road to towards targeted therapies.
The April 2011 issue of Nature Chemical Biology reports the development of a selective inhibitor of leucine-rich repeat kinase 2 (LRRK2), a gene that is mutated in some patients with Parkinson’s disease.
The team of researchers from Dana-Farber Cancer Institute, Harvard Medical School, University of Dundee, Scripps Research Institute and ActivX Biosciences applied a novel, screening strategy focused on selectively inhibiting LRRK2.
Biotech Strategy Blog recently had the privilege to interview Dr Todd Sherer, Chief Program Officer of the Michael J. Fox Foundation.
In the second part of a two-part interview, Pieter Droppert asks what the future holds for Parkinson’s disease research? You can read the first part of the interview here.
Part 2: Understanding Parkinson’s disease
Biotech Strategy Blog: Why don’t we know what the cause of Parkinson’s disease is?
Next week, I will be posting the second part of the interview that discusses the significant research the foundation is funding on biomarkers that can help the diagnosis of the disease and monitor its progression.
If you are interested in learning more about the latest developments around Parkinson’s disease biomarkers, then you may wish to consider the April 27, 2011 webinar from the American Association for the Advancement of Science (AAAS) on the “Early Detection of Parkinson’s Disease: The Challenges and Potential of New Biomarkers.”
Biotech Strategy blog recently had the privilege to do a phone interview with Dr Todd Sherer, the Chief Program Officer of the Michael J Fox Foundation. In this two- part interview, Pieter Droppert asks what the MJFF approach to research funding is and what the future holds for Parkinson’s disease research?
Part 1: Research Funding
Research funding is key to science. Without it there would be no translational medicine that takes basic research and turns it into clinical applications that benefit humans. One organization that is making a difference and bridging the gap between patients and research is the Michael J Fox Foundation (MJFF).
Taxanes are a class of drug that are used in breast, lung and ovarian cancer chemotherapy to disrupt the function of microtubules that are essential to cell division. They include paclitaxel (Taxol®) and docetaxel (Taxotere®).
Paclitaxel is also used to prevent the narrowing (restenosis) that occurs with coronary artery stents that are used to open blocked coronary arteries. Drug coated stents (a.k.a. “drug-eluting stents) reduce scar tissue.
Research published in the February 18, 2011 edition of Science, by Farida Hellal and colleagues has now shown that treatment with paclitaxel reduces the scarring associated with spinal cord injury (SCI) and promotes nerve regeneration.
Earlier this month the Michael J Fox Foundation (MJFF) announced that Vancouver based Allon Therapeutics had been able to improve motor function and brain pathology in a mouse model of Parkinson’s disease (PD).
What makes this data interesting is that it adds further support to the potential efficacy of the company’s lead product, davunetide, in a wide range of neurodegenerative disorders.
Davunetide (AL-108) is a microtubule-interacting peptide based on an eight amino acid sequence, Asn-Ala-Pro-Val-Ser-Ile-Pro-Gln, single letter code NAPVSIPQ (NAP) derived from activity-dependent neuroprotective protein (ADNP). It has been shown to have neuroprotective properties.