This is an important discovery! Jean-Marc Sabatier describes here for the first time the direct link that exists between the dysfunctional renin-angiotensin or RAS system (because it is made overactive by the viral and possibly vaccinal Spike protein) and the (possible) onset of the neurodegenerative Alzheimer’s disease on the host.
By Jean Marc Sabatier
The SARS-CoV-2 virus causes the overactivation and disruption of a central physiological system for the functioning of the human body: the renin-angiotensin system or ARS (also called the angiotensin-aldosterone system or RAAS). The ARS is responsible for autonomic (automatic) renal, lung, and cardiovascular functions; it also regulates innate immunity and the various microbiota (microbial flora of the body). RAS is ubiquitous in the body, being present in cells of various tissues and organs. The dysfunctional RAS (because it is overactive) is directly responsible for Covid-19 pathologies via the excess of the hormone angiotensin-2 which overactivates the RAS’ “harmful” AT1R receptor.
Activation of cell signaling
Indeed, the AT1R receptor that has become overactive due to angiotensin-2 excess has many harmful activities for the human body, via triggering cellular signaling cascades. The AT1R receptor is pro-hypertensive (it induces vasoconstriction of blood vessels), pro-inflammatory (it causes a harmful storm of pro-inflammatory cytokines), pro-oxidant (it increases the production of reactive oxygen species that kill cells), pro- thrombotic (it promotes the formation of blood clots – or thrombi – that clog the blood vessels), pro-angiogenic (it promotes the growth of blood vessels and tumors), pro-hypoxemic (it reduces the oxygen load of red blood cells and induces desaturation of the blood in dioxygen), pro-hypoxic (it causes a deficiency in the supply of various cells, tissues and organs in dioxygen), pro-fibrosis (it causes organ fibrosis), pro-hypertrophic (it increases the volume of organs), and lowers nitric oxide ( it affects inflammatory, immune and memory phenomena).
Neurodegenerative Alzheimer’s Disease: What’s Going On?
Alzheimer’s disease is a form of dementia characterized by disabling neurological disorders that affect the behavior, memory, thinking and reasoning abilities of those who suffer from it. The symptomatology is generally slow (but can be abnormally fast in the case of Covid-19 and long Covid). Patients mainly present with memory loss (amnesia), spatio-temporal confusion, mood and personality disorders, inability to understand and/or solve problems, impaired written and/or oral expression (aphasia), and difficulty performing daily tasks . There is a limitation in the ability to perform motor activities even though these functions are “intact” (apraxia), as well as difficulty identifying everyday objects even though the sensory functions are also “intact” (agnosia). This decline in mental function during Alzheimer’s disease is currently characterized by seven evolutionary stages, ranging from an absence of impairment to profound cognitive impairment (memory, orientation, language, attention, praxis, gnosis, executive functions, and visual skills).
50 million people worldwide
Alzheimer’s disease – which affects about 50 million people worldwide – occurs mainly in people over the age of 65 (4 to 5% of Alzheimer’s disease cases are found before the age of 65). The medical treatments developed to date to slow and counteract the degenerative process of Alzheimer’s disease aim to prevent the formation of amyloid plaques between neurons and tau protein aggregates.
The tau protein is present in the axons of neurons: it is associated with microtubules and works by regulating their dynamics. Thus, the tau protein is linked to neurofibrillary degenerations that occur in the neurons themselves. The (post-translational) modifications of the tau protein, such as acetylation or phosphorylation, make it possible to regulate its intracellular activity on the microtubules (the latter correspond to filaments of the cytoskeleton – hollow cylinders composed of tubulin – involved in various functions importance, including intracellular transport and cell division or mitosis).
Overactivated RAS (by SARS-CoV-2 or the vaccine’s spike protein), Covid-19 and Alzheimer’s disease: what’s the link?
Cases of Alzheimer’s disease have been observed (by clinicians and pathologists) in humans (including young adults), following natural infection with SARS-CoV-2 (or even an anti-Covid-2 vaccination).19) of it. As mentioned earlier, a viral infection with SARS-CoV-2 (or sometimes even an anti-Covid-19 vaccine) causes dysfunction of the ARS, via an excess of the hormone angiotensin-2 (normally broken down by the receptor ACE2- enzyme of conversion of angiotensin-2- to which the viral or vaccine spike protein binds) and the “harmful” overactivation of the AT1R receptor (of the RAS), at the origin of Covid-19 diseases. The overactivated AT1R receptor is prohypertensive, that is, it causes high blood pressure. This affects brain function.
Indeed, arterial hypertension is clearly identified as an important factor in mild or severe neurodegenerative disorders such as dementia and Alzheimer’s disease. RAS inhibitors (e.g. sartans, ACE inhibitors of the angiotensin-1 converting enzyme) have been shown to have beneficial effects on neurodegenerative diseases and other cognitive disorders (these beneficial effects are far superior to those of other known types of hypertensive drugs) . Thus, excess of the hormone angiotensin-2 is associated with neurological disorders, including a deficit in the acquisition of spatial memory. These neurological impairments and changes in cognitive function are associated with an accumulation of amyloid beta proteins in the cerebral cortex, as well as damage (decrease in synaptic content) of the hippocampal perforating pathway that connects to the entorhinal cortex (the axons/perforating fibers from the entorhinal cortex are the pathway for information to enter the hippocampus, a trisynaptic neural circuit; they contact the granule cells of the dentate gyrus), which are hallmarks of Alzheimer’s disease.
The vasoconstrictive effect of dysfunctional RAS
For example, angiotensin-2 (excess in Covid-19) and the over-activation of RAS (responsible for Covid-19 diseases) promote the accumulation and deposition of beta-amyloid proteins (markers of Alzheimer’s disease), causing the synaptic connections of brain cells and cognitive functions change. functions. In addition, the vasoconstrictive effect of dysfunctional RAS contributes to limiting cerebral blood flow, promoting neurovascular disconnection, cerebral hypometabolism and the occurrence of neurological damage.
How to limit/treat neurological (e.g. Alzheimer’s disease) and cardiovascular damage associated with RAS dysfunction?
Interesting are the different molecules (quercetin, melatonin, thymoquinone, dexamethasone, sartans, ACE inhibitors, etc.) that inhibit the overactivation of the RAS, and in particular vitamin D that acts as a brake on the RAS, with beneficial effects – among others – on the incidence of neurodegenerative diseases, cognitive disorders and cerebrovascular accidents.
Finally, I describe here for the first time that there is a direct relationship between the dysfunctional renin-angiotensin or RAS system (because it is made overactive by the viral and possibly vaccinal spike protein) and the (potential) occurrence of the neurodegenerative disease of Alzheimer’s. at the host. And certainly other degenerative diseases.
Covid: collection of censored articles by Jean-Marc Sabatier in English and Spanish