ROAD TO THE CURE UPDATE AUGUST 2017

The results are ground-breaking Alpha-Synuclein and Multiple System Atrophy. The often misdiagnosed as Parkinson’s, Multiple System Atrophy (MSA) is a rapidly progressive, fatal neurodegenerative disorder. The disease typically affects individuals between the age of 50 and 75 years of age and is characterized by a combination of autonomic dysfunction and motor abnormalities. The disease causes rapid deterioration of the central nervous system with a median survival of 6-10 years. The incidence rate is 3 per 100,000 individuals annually. In 2007, MSA disease was divided into two categories: MSA-P and MSA-C. MSA-P denotes patients predominantly exhibiting Parkinson’s-like symptoms, including postural rigidity and instability, bradykinesia, and tremor. MSA-C encompasses patients with more prominent cerebellar symptoms, including gait and limb ataxia (the loss of full control of bodily movements) with cerebellar dysarthria (difficult or unclear articulation of speech that is otherwise linguistically normal) associated with oculomotor dysfunction (a fairly common eye problem in which people are unable to follow a moving object accurately or unable to quickly shift their eyes from one point of fixation to another (saccadic fixation is necessary for tracking skills while reading or copying).

In addition to the parkinsonian and cerebellar manifestations, patients with MSA may also exhibit other neurological abnormalities, such as pyramidal signs and stupor. Autonomic manifestations may include a wide range of symptoms, such as cardiovascular, genitourinary (relating to the genital and urinary organs), and thermoregulatory (a process that allows your body to maintain its core internal temperature), but the defining autonomic features are orthostatic hypotension or autonomic urinary abnormalities. Like Parkinson’s disease (PD), the neurodegenerative MSA disease rises from the misfolding and accumulation of the protein alpha-synuclein in glial cells that surround and provide support to neurons. Alpha-synuclein aggregates isolated from MSA patient samples were shown to infect cultured mammalian cells and to transmit the neurological disease to transgenic mice. These findings argue that alpha-synuclein becomes a prion (prions are infectious agents composed entirely of a protein material that can fold in multiple, structurally abstract ways, at least one of which is transmissible to other prion proteins, leading to disease in a manner that is epidemiologically comparable to the spread of viral infection. A 2015 study concluded that multiple system atrophy (MSA), a rare human neurodegenerative disease, is caused by a misfolded version of a protein called alpha-synuclein, and is therefore also classifiable as a prion disease ) in MSA patients, similar to its role in Parkinson’s patients.

It is for this reason that both MSA and PD are classified as prion-like diseases. Thus, there is an overwhelming evidence that alpha-synuclein is the common pathological target for MSA and PD. Neuronal loss in the substantia nigra of MSA patients is similar as in PD patients. Medicinally, while Levodopa provides transient symptomatic relief to Parkinson’s patients, it provides a very poor response with MSA patients. Like other neurodegenerative diseases, a definite diagnosis of MSA can only be made upon autopsy by the presence of misfolded alpha-synuclein in glial cells, the pathological landmark of the disease, along with neurodegenerative changes in the striatonigral structures in an individual’s brain. The diagnosis of possible MSA is based on the presence of either parkinsonian or cerebellar symptom in patients, with at least one feature of autonomic and/or urogenital dysfunction, plus one other clinical feature (such as a Babinski sign with hyperreflexia) in patients over the age of 30 presenting with progressive disease.

Probable MSA patients, also over the age of 30, exhibit rapidly deteriorating autonomic activity with urinary dysfunction and either poor levodopa-responsive parkinsonism or cerebellar dysfunction. Unfortunately, currently, there are no therapies available that can slow down and/or halt the MSA disease progression. Current treatments are focused on symptom alleviation, but these treatments typically offer only partial and transient relief for patients. The good news is that ICB, International, Inc., (“ICBII”), has developed a drug for Parkinson’s disease which has been shown, in animals, to inhibit the production of pathological alpha-synuclein which is the hallmark of Parkinson’s and MSA diseases. The scientists of ICBII are now in search of MSA animal models to test its drug. There is a high probability that after cloning and humanization, ICBII’s alpha-synuclein-SM will be effective in halting Parkinson’s and MSA diseases. The Company is now looking for investors to raise funds to achieve its goal of translating its drug for human use.

HOW CAN YOU HELP? The joy of being a part of this historical event can be had by helping ICBI find the funds to bring these trials to fruition through your personal, including your IRA, investment, and/or by finding others with the financial ability and humanitarian mindset to accomplish the - until now - impossible. Please contact Jo Rosen at Parkinson’s Resource Organization 760-773-5628 or jo rosen@Parkinsonsresource.org or by contacting ICBI directly through their website http://icbii.com/ or by phone 858-455-9880. IMAGINE the world without Parkinson’s, MSA or Alzheimer’s disease. JUST IMAGINE. Mark your calendars and join us at the Parkinson’s Resource Organization “On the Road to the Cure” symposium October 28th in Palm Desert, California.