Epidemic of modern times: Alzheimer’s Disease
Alzheimer’s disease results in a slow but sure destruction of the mind and body. It makes you unable to take care of yourself and interact with the world around you. It steals away the very essence of what it means to be human, and ultimately, it kills you (Mucke 2009).
Those who are diagnosed with Alzheimer’s often see no light at the end of the tunnel, as there is currently no treatment or cure for this terrible disease. But not anymore. Our research team, lead by Dr. Yuri Zilberter, has been working on a new approach in the fight against Alzheimer’s, with great promise to stop/prevent, and potentially even reverse/cure the disease, which can hopefully provide Alzheimer’s patients with a glimmer of hope for the future.
Meet the killer
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 comorbid with other neurodegenerative diseases, including epilepsy (Palop & Mucke 2009), and has an endless list of risk factors which include tumours, 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.
35 million sufferers
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.
$600 billion annual cost
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 new direction in Alzheimer’s research
The Metabolism and Neuroprotection Research Group at Aix-Marseille University in France headed by Dr. Yuri Zilberter leads a new direction in Alzheimer’s research. The preliminary findings of our multidisciplinary worldwide team promise to be revolutionary.
To help you understand the groundbreaking nature of our approach, let us briefly review the modern state of Alzheimer’s research.
Old approach is spinning wheels
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.
So the $600 billion dollar question is:
What is the fundamental underlying mechanism that causes AD?
Our answer to the $600 billion question
We propose that this mechanism is a deficiency in energy supply to the brain, a metabolic crisis that triggers the pathology of AD and many other neurodegenerative disorders. If we correct the underlying problem, we can stop the disease before it develops.
The logic is simple: No problem, no disease
The connection between brain energy metabolism and AD is not a new idea, but it has been widely underestimated for years and little research has been done into correcting the problem. For the past 9 years our team has been on a quest to systematically uncover the mysteries of the relationship between brain metabolism and neurodegenerative diseases.
We have uncovered something extremely exciting
In our recent results we have found a way of correcting this problem, outlining a method of preventing and halting AD pathology, as well as potentially reversing it altogether.
As described earlier, we believe the trigger to the pathogenesis of many neurodegenerative diseases to be a deficit in energy supply to brain cells, and thus many of these diseases may be comorbid. Of particular interest to us, is the comorbidity of AD and epilepsy. Why? Because one of greatest the barriers to researching AD is that there are still no early diagnosis, and thus signals to examine. Analysis of medical data show a high correlation between AD and epilepsy; i.e the medical history of AD patients often exhibited epileptic symptoms decades prior to their AD-diagnosis. This is evidence that the spontaneous outbreak of epileptic symptoms (i.e. not genetic) is one of the earliest symptoms/signs of AD pathology (Palop & Mucke 2009, Noebels 2011, Bakker et al. 2012).
It is reasonable to use epilepsy as a marker for an increased likelihood of AD, because the two diseases are likely both caused by energy deficiency. The key here is that epilepsy is easy and cheap to detect and diagnose early on, using EEG brain scanning techniques. The main feature of epilepsy is a hyperexcitability of brain cells (which causes its symptoms, e.g. seizures). In AD, this hyperexcitability is caused by overproduction of Aβ at very early stages in AD-pathology, far before the formation of clusters (as stated in the Amyloid Hypothesis, mentioned earlier).
In our research, we have used this hyperexcitability in epilepsy/AD (as detected by EEG-like brain scanning techniques) and have linked it to the mechanism thought to be involved in triggering the pathology of neurodegenerative diseases, i.e. brain energy supply.
Here comes Pyruvate
We have found that there is indeed a link between the two and that by using energy substrate called Pyruvate as a dietary supplement, the toxic effect of Aβ-overproduction is absent (verified by absence of neural hyperexcitability, damage to synaptic function and energy deficiency).
We have found that pyruvate supplementation interrupts the vicious cycle caused by metabolic crisis in the brain, by correcting the underlying energy supply deficiency which triggers AD pathology. Pyruvate is completely safe with no side effects and it is sold over-the-counter across the globe. Furthermore, it is completely natural (it is produced by your own body) and nothing artificial is added. Essentially, it is a fuel source for brain cells.
Thus, it makes sense that if there is a deficiency in energy provided to the cells, taking supplements of pyruvate, the fuel itself, 'corrects' the faulty metabolism that triggers AD. What is exciting about this is that it is unlike many other drug trials where the substances used are just that, drugs. In this case it’s a simple dietary supplement, its cheap, and our results show real promise for success in preventing AD. We are very excited to investigate this more, as this approach may prove to be revolutionary in AD research/treatment development and hopefully we can contribute to the battle against this terrible disease.
We need results quickly!
AD is a trending topic and there are literally thousands of scientific articles being published every year. We have launched this campaign in order to ensure that our promising results are not lost in the sea of AD research, as we believe it is extremely important that people hear about this approach.
The main issue at hand is that AD is getting worse and we need results quickly! Besides continuing our research into the metabolic correction of AD, we aim to raise awareness of this approach to both the scientific community as well as the lay public, as this problem concerns us all, and the potential implications/benefits of this approach may prove to be enormous. By raising awareness, we also aim provide a little hope to the millions of people affected by this terrible disease, who currently believe there is no light at the end of the tunnel for both themselves and future sufferers. We sincerely hope that with further research into this approach, and with subsequent clinical trials based on it, that this could be single biggest breakthrough ever in our fight against AD and other neurodegenerative diseases.
References
- alz.co.uk/research/statistics
- Bakker, A., Krauss, G. L., Albert, M. S., Speck, C. L., Jones, L. R., Stark, C. E., Yassa, M. A., Bassett, S. S., Shelton, A. L. and Gallagher, M. (2012) Reduction of hippocampal hyperactivity improves cognition in amnestic mild cognitive impairment. Neuron, 74, 467-474.
- De la Torre, J. C. (2010) Vascular risk factor detection and control may prevent Alzheimer's disease. Ageing Res Rev, 9, 218-225.
- Huang, Y. and Mucke, L. (2012) Alzheimer mechanisms and therapeutic strategies. Cell, 148, 1204-1222.
- Karran, E., Mercken, M. and De Strooper, B. (2011) The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics. Nat Rev Drug Discov, 10, 698-712.
- Mucke, L. (2009) Neuroscience: Alzheimer's disease. Nature, 461, 895-897.
- Noebels, J. (2011) A perfect storm: Converging paths of epilepsy and Alzheimer's dementia intersect in the hippocampal formation. Epilepsia, 52 Suppl 1, 39-46.
- Palop, J. J. and Mucke, L. (2009) Epilepsy and cognitive impairments in Alzheimer disease. Archives of Neurology, 66, 435-440.
- Patterson, C., Feightner, J., Garcia, A. and MacKnight, C. (2007) General risk factors for dementia: a systematic evidence review. Alzheimers Dement, 3, 341-347.
- Saxena, U. (2010) Alzheimer's disease amyloid hypothesis at crossroads: where do we go from here? Expert Opin Ther Targets, 14, 1273-1277.
- Zilberter, M., Ivanov, A., Ziyatdinova, S., Mukhtarov, M., Malkov, A., Alpar, A., Tortoriello, G., Botting, C. H., Fulop, L., Osypov, A. A., Pitkanen, A., Tanila, H., Harkany, T. and Zilberter, Y. (2013) Dietary energy substrates reverse early neuronal hyperactivity in a mouse model of Alzheimer's disease. J Neurochem, 125, 157-171.