Our concept: metabolic crisis triggers a vicious circle, which can be stopped by metabolic correction

We are developing a method that will allow humanity to prevent, stop and reverse aging-related cognitive decline including Alzheimer’s disease.  In our most recent study we demonstrate that there is a way to correct this pathology and stop the progression of Alzheimer’s. But we aim to not only stop the progression  but prevent the neurodegenerative diseases of aging altogether.

First identified by Alois Alzheimer in the early 1900’s, Alzheimer’s Disease (AD) is the prevailing age-related neurodegenerative disorder today. While AD is most commonly associated with dementia and memory loss, it also affects many other functions. It is highly co-morbid with other neurodegenerative diseases, including epilepsy (Palop & Mucke 2009), and has an endless list of risk factors which include tumors, diabetes, cardiovascular diseases and infections (de la Torre 2010; Patterson et al. 2007). Despite a wealth of knowledge and research, humanity still has no early diagnosis and no treatment, let alone a cure for AD.

There are approximately 35 million people suffering from this terrible fate worldwide. If dementia were a country, it would be around the 35th largest by population in the world, larger than Canada. With a growing population of elderly people, the problem is going to get much, much worse. These numbers are expected to increase dramatically, with estimates ranging from 65 million by 2030 to 115 million by 2050. The suffering is not limited to the Alzheimers patients, as their families, loved ones and caregivers are also put under great emotional and physical burdens.

Not many people are aware of the financial burden AD exerts on society, entire healthcare systems and common taxpayers. In 2010, it was estimated that the worldwide financial cost of AD exceeded $600 billion, the monetary equivalent of the 18th largest economy in the world, between Turkey and Indonesia (alz.co.uk).

The predominant theory of the pathogenesis of AD, and thus also the basis of drug trials, has been the so-called Amyloid Hypothesis (Karran et al. 2011). Amyloid Beta (Aβ) is a peptide that is produced by our brains. It occurs naturally in healthy brains but only in small concentrations that aren’t harmful. In large concentrations, however, Aβ has a very toxic effect and forms clusters – so called neurofibrillary tangles or amyloid plaques.  According to the classic Amyloid Hypothesis, the overproduction of Aβ which leads to the formation of toxic clusters is the cause of cognitive decline, the primary symptom of Alzheimer’s Disease. Based on this theory, most existing AD research and drug trials focused on (Saxena, 2010; Karran et al., 2011; Huang & Mucke, 2012):

  • Mechanisms involved in Aβ production
  • Processes involved in the formation of Aβ clusters
  • Elimination of the Aβ clusters

Unfortunately, all drug trials to date have failed to show cognitive improvement and halt AD pathology. Despite all attempts, the Aβ toxicity seems to remain intact.

We asked a different question

In order to advance research concerning the prevention/treatment of AD, we must reconsider the theory regarding AD pathology. Due to the slow and progressive nature of AD it cannot be diagnosed until symptoms appear. When they do, it’s already too late to do anything about it. What else do we know? We know that AD wreaks havoc on just about every brain function. So, rather than focusing solely on the toxic effect of Aβ, we decided to look for the root cause of AD pathology. We suggest that since AD devastates such a wide array of the brains functions, it is reasonable to assume that there must be a fundamental underlying mechanism in the brain that is at fault. A mechanism that the brain cannot do without and which affects all brain functions.

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