ICBI UPDATE ON THE ROAD TO THE CURE - New Insights into Parkinson’s Disease

A protein known as the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) is a member of the innate immune receptor of the TREM family. TREM2 manifests on activated macrophages [a type of white blood cell, of the immune system, that engulfs and digests cellular debris, foreign substances, microbes, cancer cells, and anything else that does not have the type of proteins specific to healthy body cells on its surface].  It also manifests on immature dendritic cells [messengers between the innate and the adaptive immune systems]; osteoclasts [a large multinucleate bone cell that absorbs bone tissue during growth and healing]; and microglia {scavengers in the central nervous system]. The TREM2 function is to suppress inflammation while at the same time promote tissue repair through the removal of dying cells and clearance of toxic protein aggregates. Loss of function of TREM2 due to mutations in the gene leads to neurodegeneration.

In particular, the TREM2 mutation R47H has been independently identified by two different research groups as a genetic risk factor for late-onset Alzheimer’s disease. Jonson et al [NEJM, 368, 107 (2013)] used whole-genome sequencing data obtained from 2261 Icelandic individuals to identify variants likely to affect protein function. Upon imputation of these variants into a series of late-onset Alzheimer patients and controls using genome-wide association data, they showed that the R47H mutant conferred a significant, three-fold risk of the late-onset Alzheimer’s. They replicated this association across additional Alzheimer controls from Europe and the US. Additionally, independent whole-genome sequencing in Alzheimer patients by Guerreiro et al [JAMA Neurology, 70, 78 (2013)] further confirmed that Alzheimer patients have an increased burden of mutant TREM2 compared to normal controls. This study reported higher odds of the late-onset Alzheimer’s by ~4.5 fold.  Together these studies unequivocally implicated TREM2 R47H in Alzheimer’s risk; however, its role in other neurodegenerative diseases has yet to be studied.

Role of R47H Mutant TREM2 in PD - According to the study reported by Sruti Rayaprolu, et al.,  North American Parkinson’s patients had a three-fold higher prevalence of mutant TREM2 gene than the normal control [Molecular Neurodegeneration, 8, 19 (2013)]. Irish and Polish Parkinson’s patients had similar statistics of the R47H variant in TREM2 in the etiology of Parkinson’s. Thus, mutant TREM2 is implicated in Parkinson’s disease.

What Does This Information Mean? – The majority of patients, to halt and reverse Parkinson’s disease, need treatment with drugs that not only clear the toxic proteins from the brain but also nullify the effect of mutant TREM2 for providing maximum health benefits. THE GOOD NEWS is that ICBII has developed the technology of a blood-brain barrier permeable SMART Molecule that will target alpha-synuclein toxic protein clumps and mutant TREM2 in the central nervous system. The Company is very excited to start developing and manufacturing this potentially revolutionary drug to halt and reverse Parkinson’s. 

WOULD YOU LIKE TO HELP get these drugs to market faster? 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 investing, including your IRA, and by finding others with the financial ability and humanitarian mindset to accomplish the - until now - impossible. Please contact Parkinson’s Resource Organization 760-773-5628 or info@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.