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A gold nanocrystal drug called CNM-Au8 significantly reversed brain energy deficits and motor functions in patients suffering from multiple sclerosis (MS) and Parkinson’s. These pathologies are in fact characterized by rapid changes in energy metabolism at the neuronal level. After 12 weeks of daily intake, significant functional recovery was observed in all patients.
The functioning of our organs, including the brain, depends on a constant supply of energy supplied to the cells by the mitochondria in the form of adenosine triphosphate (ATP). The efficiency of energy metabolism decreases with age and leads to a deficiency in ATP availability in neurons. Research shows that this deficiency is exacerbated in neurodegenerative diseases and can often be detected before clinical symptoms appear.
In neurodegeneration, impaired energy metabolism leads to oxidative and neuroinflammatory stressors as well as proteostatic decline (impairing protein stabilization). These factors in turn trigger a vicious circle, which induces further energy deficiency and neurodegeneration. They contribute to the accumulation of toxic proteins characteristic of neurodegenerative diseases, such as beta-amyloid protein and tau protein in the case of Alzheimer’s.
Neurodegenerative pathologies also lead to a rapid and severe decrease in the nicotinamide adenine dinucleotide (NAD) ratio. +) and nicotinamide adenine dinucleotide hydrogen (NADH). These are pairs of enzymatic cofactors required for cellular reactions leading to the synthesis of ATP. They are also involved in many functions, such as the regulation of intracellular energy uptake and nutrient availability. As a result N.A.D +/NADH is considered an indicator of the overall energy capacity of the brain.
Previous research has suggested that preventing or reversing energy deficits may slow the progression of neurodegenerative diseases. Recently one suggested regenerating mitochondria to treat Alzheimer’s.
Strategies targeting energy metabolism may lead to partial recovery, according to researchers at the University of Texas Southwestern (UTSW). Together with the biopharmaceutical company Clean Nanomedicine, they proposed a new approach directly impacting the NAD report. +/NADH, by specially developed gold nanocrystals.
A phase 2 clinical trial of the drug, called CNM-Au8 – described Journal of Nanobiotechnology – Show promising results for MS and Parkinson’s. ” We are cautiously optimistic about our ability to prevent or even reverse some neurological disorders with this strategy. Peter Sgugna, assistant professor of neurology and researcher at UTSW’s Peter O’Donnell Jr. Brain Institute, said in a statement.
Functional improvement after 12 weeks
Gold nanocrystals developed by researchers in the new study act as catalysts, increasing the NAD ratio. + /NADH in neurons. Administered orally as a concentrated suspension, these particles can cross the blood-brain barrier and catalyze the rapid oxidation of NADH to NAD+. This reaction increases the intraneuronal availability of NAD+ and ATP.
During the previous tests in vitro And preclinically, CNM-Au8 has been shown to restore energy homeostasis and reduce oxidative stress in neurons. The treatment also led to the reinnervation of damaged axons. Additionally, “while gold nanoparticles have been shown to have the ability to act as biological catalysts, to our knowledge, CNM-Au8 is the only suspension of gold nanocrystals that exhibits catalytic activity and exceptionally high and very low toxicity,” the UTSW researchers suggest. In his studies.
Increased brain NAD+/NADH ratio in Parkinson’s and MS participants in repair clinical trials. (a) Changes in brain NAD + /NADH ratio and secondary endpoints, (b) Changes in NAD + fraction and changes in NADH fraction after 12+ weeks of daily administration of CNM-Au8. (c) The REPAIR-MS trial protocol provided for 6-week treatment discontinuation after 12 weeks of administration. © Jimin Ren et al.
As part of a phase 2 clinical trial for CNM-Au8, 11 MS and 13 Parkinson’s volunteers were recruited. To assess the effects, participants underwent magnetic resonance spectroscopy of the brain before and after treatment. The drug was administered daily for 12 weeks.
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In all patients, the drug increased the NAD ratio by 10.4% +/NADH compared to their initial values. This is a significant therapeutic effect, given that (healthy) aging causes a loss of approximately 0.5% in the brain’s NAD ratio. +/NADH every 10 years. Participants also reported significant improvements in their motor functions. No significant side effects have been reported.
According to experts, the improvement achieved with CNM-Au8 should be enough to potentially reverse neurodegeneration rather than slow it down like current treatments. The drug can also be applied to other neurodegenerative diseases. However, additional research will be needed to assess the reproducibility of the results, particularly in progressive MS (characterized by regular and rapid worsening of symptoms).
Video explaining how the CNM-Au8 works:
Source: Journal of Nanobiotechnology
