ICBII Update on the Road to the Cure -- August 2023

Mitochondria Dysfunction and Neurodegeneration

Recently, there has been a lot of media coverage on humanized mouse monoclonal antibodies that have been FDA approved for treating early-stage Alzheimer’s  patients. These antibodies are Aduhelm (Biogen), Lecanemab (Biogen/Eisai), and Donanemab (Lilly) that slowed cognition decline in early-stage AD patients. The reported “slow decline”, for example, in the case of Biogen’s Aduhelm was 27%. The reality is that, during the treatment period, cognition worsened by 73% when compared with the baseline cognition that went down 100% with a placebo. In our opinion, these antibodies don’t represent a potential cure, that will give Alzheimer patients their memory back. 

Why is there still no cure for most of the neurodegenerative diseases?

It would be naïve to say that the science understands every reason and faulty mechanism that may be the root cause of diseases like Alzheimer’s, Parkinson’s, and many others. The most common culprits appear to be: 1) Impermeability of the blood-brain barrier (BBB). For example, ~ 98% of all drugs cannot reach the central nervous system; 2) Lack of understanding about the cause of neurodegeneration. For several decades, protein aggregation such as amyloid-beta in case of Alzheimer’s and alpha-synuclein for Parkinson’s has been attributed as causative. However, no direct relationship has been documented between the amount of protein aggregation in the brain and decline in cognition and motor function. Age-matched healthy individuals have been found to have protein aggregation in their brains but without symptoms of Alzheimer’s, or Parkinson’s.   

Recent advances in brain sciences have discovered that the disease manifestation in Parkinson’s and Alzheimer’s patients starts 10-20 years before the appearance of protein aggregation and symptoms. Evidence points out Mitochondria Dysfunction. 

What are Mitochondria?

Mitochondria are the primary source of energy production in neurons, supporting the high energy consumption of the nervous system. They are cytoplasmic organelles responsible for life and death. Extensive evidence from animal and clinical studies suggests that mitochondria play a critical role in aging, cancer, diabetes, and neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, Huntington’s, and many other diseases. Several lines of research suggest that mitochondrial oxidative damage is an important cellular change in most late-onset neurodegenerative diseases. Further, emerging evidence suggests that structural changes in mitochondria, including increased mitochondrial fragmentation and decreased mitochondrial fusion, are critical factors associated with mitochondrial dysfunction and cell death in aging and age-related diseases.

It is inconceivable that anyone can cure or even slow down the progression of neurodegenerative diseases without correcting mitochondria function. Next month, we will write on potential approaches to restoring mitochondria function.

WOULD YOU LIKE TO HELP get ICBII’s drugs to market faster? The joy of being a part of these historical events 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 or by phone 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.