LSD and Covid (Part 2)

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LSD and Covid (Part 2)

LSD stands for Lysosomal Storage Disorders and the first part can be found hereThe disorder is otherwise known as Fabry disease and although the lysosome is a separate organelle it’s signalling pathways connect to the mitochondria.

The Dichotomous Role of Inflammation in the CNS: A Mitochondrial Point of View

The main causes of NLRP3 inflammasome activation in ischemic conditions are ascribable to mitochondria dysfunction, as abnormal Ca2+ influx, ROS production, mitochondrial membrane permeabilization with the consequent release of DAMPs and mtDNA, all conditions that are tightly linked one to the other (Figure 3). Within minutes, OGD affects mitochondria functions leading to a strong reduction of OXPHOS and therefore of ATP synthesis. Neurons in the infarct core fail to compensate the ATP cell request leading to a bust of the Na+/K+ ATPase pump [185,192]. This results in neuronal membrane depolarization accompanied by an extreme release of glutamate in the extracellular space finally leading to neurons loss [193]. Glutamate is an important excitatory neurotransmitter, which binds several types of receptors such as N-methyl-D-aspartate (NMDA) receptor, a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor and kainate receptor [194]. Although these receptors originally were thought to be exclusive to neurons, several studies revealed their functional expression also on glial cells [195,196]. The excessive amount of glutamate after stroke leads to a hyperactivation of these receptors promoting a strong influx of Ca2+ into the cells [197,198,199]. Mitochondria are the crucial players in regulating cytosolic Ca2+ levels [200], thus the massive accumulation of cytosolic Ca2+ results into the activation of the mitochondria calcium uniporter (MCU) leading to mitochondrial depolarization, which in turn drives NLRP3 inflammasome activation and the consequently IL-1β release [201]. Consistently, it has been found that in response to the activation of NMDA receptors, MCU overexpression increases mitochondrial Ca2+ levels and provokes mitochondrial membrane depolarization. Inversely, genetic knockdown of MCU reduces the NMDA-induced increase in mitochondrial Ca2+ followed by lower levels of mitochondrial depolarization [202]. In line with these findings, in focal cerebral ischemia rat models, the early stages of cerebral ischemia are characterized by an upregulation of the mitochondrial calcium uptake 1 (MICU1) a crucial regulator of MCU [203]. Interestingly this occurs in the acute phase of IS right when the inflammatory response takes place [204,205,206]. To corroborate the role of Ca2+ in mitochondria dysfunction-induced inflammation, it has been shown that NLRP3 inflammasome activation is reduced following the inhibition of extracellular Ca2+ entry or the depletion of Ca2+ stores in the ER [207]. Albeit K+ efflux, a common NLRP3 inducer [208], has been proposed to be upstream of the Ca2+-induced NLRP3 inflammasome activation, thus indicating that high levels of extracellular K+ abolish NLRP3 activation [209], the crucial contribution of mitochondrial Ca2+ overload in sustaining inflammasome activation following IS and IR is not excluded.

I found this infomercial  promoting a supplement for nerve regeneration and thought it was very good so I cut it into segments and placed the links in the tweets. I was already using N-acetylcysteine (NAC) and had ordered Niacin and α-lipoic acid (A-ALA) and R-lipoic acid (R-ALA) which I have just started taking.  The one thing that seems to work across all the mitochondrial diseases is  Co-enzyme 10 (CoQ10) which I just bought today.


This Review (see page 15) more or less confirms what the infomercial said. These are the supplements mentioned (some are still being trialed).

Co-enzyme 10 (CoQ10)
CoQ10 analogue, idebenone
N-acetylcysteine (NAC)
α-lipoic acid (A-ALA)
R-lipoic acid (R-ALA)
Genistein, a natural isoflavone
synthetic quinone, EPI-743
Thiamine (vitamin B1)
Elamipretide is an aromatic cationic tetrapeptide

Some of the synthetics (EP-743) mentioned above:

Many of these compounds can be found in natural food. Trehalose is found in Mushrooms, yeast, honey, and shellfish all contain trehalose but their combined dietary contribution is low in comparison to added sugars in processed foods. They have started adding it to food which causes other problems. The other compounds increased the reporter activity of GAL4-PGC-1β: Genistein, daidzein, and resveratrols stimulate PGC-1β-mediated gene expression. They can be found in high soy products dark chocolate and red wine. Let food be your medicine.

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The way forward is eating healthy and walking more and experimenting with the different supplements that boost mitochondrial health.  Intermittent fasting is also good. Meditation and positive thinking. Everything is in the hands of the Almighty and remember this…. your ancestors whose defects you inherited walked  this earth for generations.  They lived, built homes, had children and died.  We  are more than a collection of genes and our destiny through grace is eternal life.