CONTINUATION OF THE ROLE OF NEURO-INFLAMMATION IN PARKINSON’S DISEASE · Parkinson's Resource Organization

CONTINUATION OF THE ROLE OF NEURO-INFLAMMATION IN PARKINSON’S DISEASE

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UPDATE ON THE ROAD TO THE CURE

A REAL-TIME SCIENCE REPORT

CONTINUATION OF THE ROLE OF NEURO-INFLAMMATION IN PARKINSON’S DISEASE

 

“ICBII” has developed a novel class of antibodies that has been confirmed to very efficiently migrate through the BBB…

Last month we discussed the role of neuro-inflammation in Parkinson’s disease. We discussed that microglia is one of the major cell types in the brain, which are involved in the inflammatory responses in the central nervous system (CNS). McGeer et al. showed in 1988 the presence of highly reactive microglia in the substantia nigra portion of human post-mortem brain tissues, which was the first unequivocal evidence supporting the involvement of neuro-inflammation in Parkinson’s pathogenesis [Neurology, 38, 285 (1988)]. Furthermore, positron emission tomography (PET) studies also indicated that there is pronounced activation of microglia in the various regions of Parkinson’s disease brain and animal models [Parkinsonism Related Disorder, 16, 57 (2010); Front Cell Neurosci., 7, 53, (2013)]. As stated last month, neuro-inflammation in the brain results due to either a physical and/or chemical injury to the brain which may be in the form of striking head against some object or aberrant accumulation of alpha-synuclein in the brain, respectively.

ICBII Approach to Neutralize Neuro-inflammation Given the important role of neuro-inflammation in the initiation and progression of Parkinson’s disease, it is highly appropriate to develop intervening therapies for this devastating disorder by targeting the inflammatory pathways mediated by activated glial cells. For example, soluble tumor necrosis factor alpha (TNF-α) is known to contribute to the progressive degeneration of dopamine producing neurons in rodents induced by stereotactic injection of 6-hydroxydopamine (6-OHDA) or LPS. Overexpression of dominant-negative TNF-α specifically inhibits TNF signaling in the substantia nigra and attenuates activation of microglia, thereby reducing loss of dopamine producing neurons and improving locomotor ability in 6-OHDA induced rat PD model [Molecular Ther, 19, 46 (2011)].

TNF-α-SMART Molecule (TNF-α-SM) – The global scientific community has developed classical mouse monoclonal antibodies to inhibit the deleterious effect of soluble TNF-α. Unfortunately, these antibodies did not cross the blood brain barrier (BBB) into the central nervous system, so the patients were not benefitted. However, La Jolla based ICB International, Inc., (“ICBII”) has developed a novel class of antibodies that has been confirmed to very efficiently migrate through the BBB into the brain. Plans for developing TNF-α-SM are underway. In fact, our goal is to kill two pathogens with one SMART Molecule carrying an antibody for oligomeric α-synuclein on one end and TNF-α antibody on the other end of the same SMART Molecule. 

  In addition to TNF-alpha, there are several other pro-inflammatory mediators that stimulate the activation of glial cells. A handful of them are Interleukin-1 and Interferon-gamma. Attenuation of their activity may also be necessary if it turns out that attenuating the function of TNF-α alone does not provide adequate health benefits to Parkinson’s patients. 

Would You Like To Help get ICBII’s drugs to market faster? The joy of being a part of this historical event can be had by helping ICBII find the funds to bring these trials to fruition through your investing, and by finding others with the financial ability and humanitarian mindset to accomplish the —until now—impossible. Please contact ICBII directly through their website icbii.com, by phone at 858-455-9880, or contact Jo Rosen at PRO for a personal introduction to the scientists.

Imagine the world without Parkinson’s, MSA, or Alzheimer’s disease. 

JUST IMAGINE.

 

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Updated: August 16, 2017