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ALS Worldwide
February 22, 2016

MicroNeurotrophins: An Introduction


"For the first time we have a drug that targets the multiple pathways of motor neuron degeneration that are characteristic of ALS. MicroNeurotrophins protect and strengthen neurons in a variety of ways. The preliminary results of our research are very encouraging," 
Dr. James P. Bennett, Jr.
Principal Investigator, MicroNeurotrophin Research; Affiliate Clinical Professor of Neurology, Virginia Commonwealth University; President and Chief Scientific Officer, Neurodegeneration Therapeutics, Inc.


What Are MicroNeurotrophins?
The name MicroNeurotrophin comes from two words: “micro” means “small” and “neurotrophin” refers to proteins produced by the body that help nerve cells develop, grow, function, signal, and even repair themselves.

MicroNeurotrophins are small enough to cross the blood-brain barrier. By mimicking the beneficial properties of neurotrophins, they are also powerful enough to help living nerve cells affected by ALS revive and survive.

Because of these unique characteristics, MicroNeurotrophins are the first drugs that appear to counteract the multiple ways that nerve cells die in major brain diseases. They have already proven effective and non-toxic in experimental models of three major human neurodegenerative diseases: Multiple Sclerosis, Parkinson’s disease and Alzheimer’s disease. 

This initial research indicates that MicroNeurotrophins hold great promise for treating ALS/MND because they target the multiple pathways of motor neuron degeneration that are characteristic of the disease.

Addressing the multiple pathways of ALS/MND

Anti-Apoptotic
Apoptosis, programmed cell death, is responsible for motor neuron degeneration in ALS/MND. In both in vitro (cell culture) and in vivo (animal model) studies, MicroNeurotrophins have been shown to combat apoptosis by protecting and strengthening neurons.

Anti-Inflammatory and Autoimmune Inhibitor
Inflammation is the immune system’s defense against bacteria, viruses, and substances that are foreign and harmful. However, there is increasing evidence that inflammation accompanies the death of motor neurons in ALS/MND. MicroNeurotrophins’ powerful anti-inflammatory properties may help reduce, prevent, or even reverse this destructive autoimmune response.

Inflammation is the immune system’s defense against bacteria, viruses, and substances that are foreign and harmful. However, there is increasing evidence that inflammation accompanies the death of motor neurons in ALS/MND. MicroNeurotrophins’ powerful anti-inflammatory properties may help reduce, prevent, or even reverse this destructive autoimmune response.

Glutamate Modulator
ALS/MND patients are unable to properly regulate glutamate, a chemical that carries messages throughout the brain and spinal cord. Too much glutamate in the brain can be toxic and cause motor neurons to die. MicroNeurotrophins serve as an indirect protectant against excess glutamate through their ability to promote cell survival processes, increase neuronal signaling strength and as an autoimmune modulator.

Neuronal Signaling
In ALS/MND, loss of neurotrophic signaling causes neurons to die. MicroNeurotrophins prevent cell death by increasing neuroprotective signals that help neurons survive, differentiate, and grow.

The ALS MicroNeurotrophin Research Consortium:
Very encouraging preclinical results for ALS/MND 

ALS Worldwide created and funded an international group of researchers to test the effectiveness of MicroNeurotrophin drugs in treating ALS. These in vivo (animal model) and in vitro (cell culture) studies were conducted by Harvard University, Virginia Commonwealth University, The University of Sheffield, University of Crete, and Neurodegeneration Therapeutics, Inc., a nonprofit laboratory in Charlottesville, Virginia.

After rigorous pre-clinical testing, MicroNeurotrophin drugs show no signs of toxicity or harmful side effects and appear to protect and strengthen the nerve cells affected by ALS. For more detailed information about the preclinical trials, please click here.