Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease that leads to muscle weakness, paralysis and invariably has a fatal outcome. Anybody can get the disease and it is not known why some do and others don’t.
The cause of ALS is not fully understood, but it is known that many different factors and processes are involved. There have been numerous attempts to find a drug to slow down disease, but thus far without satisfying results, which is likely due to the complexity and multifactorial nature of the disease.
At Cerebro, we want to change the fatal prognosis of ALS by developing a treatment that halts the disease process and reduces ALS to a chronic disease.
Currently, anyone who is diagnosed with ALS expects the disease to be fatal within a couple of years.
It is our mission to develop and deliver a drug that will give patients a better perspective.
Cerebro is developing the promising drug candidate 4ALS, which has the potential to be a meaningful treatment in the context of ALS.
Multiple pathways are involved in the development of ALS. A history of many clinical trials has shown that addressing one pathway at a time is not sufficient to halt ALS.
We feel that a complex and multifactorial disease such as ALS should be addressed at multiple fronts at the same time.
Cerebro is developing the drug candidate 4ALS which has the potential to impact four important mechanisms underlying the development and progression of ALS.
At Cerebro Biosolutions, we feel that a complex and multifactorial disease such as ALS should be addressed at multiple fronts at the same time. Once the interplay of astrocyte activation, inflammation, and scar formation has grown to become a self-sustaining process spreading and aggravating disease, it is highly likely that addressing only the initiating cause of neuronal cell death is insufficient to significantly impact disease progress.
Cerebro Biosolutions has identified a compound that might prove a good candidate for the treatment of ALS. The compound, termed 4ALS, should impact not only the initiating process of glutamate-induced excitotoxicity, but also the secondary […]