This is a major 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 overactivated by the viral and possibly vaccinal Spike protein) and the (potential) onset of neurodegenerative Alzheimer’s disease at 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, pulmonary, and cardiovascular functions; it also controls innate immunity and the various microbiota (microbial flora of the organism). RAS is ubiquitous in the body, as it is present in cells of various tissues and organs. The dysfunctional RAS (because it is overactivated) is directly responsible for Covid-19 pathologies via the excess of the hormone angiotensin-2 which overactivates the “deleterious” AT1R receptor of the RAS.
Triggering cell signaling
Indeed, the AT1R receptor overactivated by an excess of angiotensin-2 has many harmful activities for the human body, via the triggering of cellular signaling cascades. The AT1R receptor is pro-hypertensive (it induces vasoconstriction of blood vessels), pro-inflammatory (it induces a deleterious storm of pro-inflammatory cytokines), pro-oxidant (it increases the production of reactive oxygen particles which kill cells), pro-thrombotic (it promotes the formation of clots -or thrombi- which obstruct blood vessels), pro-angiogenic (it promotes the growth of blood vessels and tumours), pro-hypoxemic (it reduces the load of red blood cells in dioxygen and induces desaturation of the blood in dioxygen), pro-hypoxic (it causes a deficit in the supply of various cells, tissues and organs in dioxygen), pro-fibrosis (it induces organ fibrosis), pro – hypertrophic (it increases the volume of organs), and lowers nitric oxide (it affects inflammatory, immune and memory phenomena).
Alzheimer’s neurodegenerative disease: what’s going on?
Alzheimer’s disease is a form of dementia that is characterized by disabling neurological disorders that affect the behavior, memory, thinking and reasoning skills of people who suffer from it. The symptomatology is generally of slow progression (but can be abnormally rapid in the event 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 expression and/or or oral (aphasia), and difficulty managing daily tasks. There is an impairment of the ability to perform motor activities even though these functions are “intact” (apraxia), as well as difficulties in identifying everyday objects although the sensory functions are also “intact” (agnosia). This decline in mental functions during Alzheimer’s disease is currently characterized by seven evolutionary stages, ranging from an absence of impairment to very severe cognitive deficit (memory, orientation, language, attention, praxis, gnosis, executive functions and visual abilities). spatial).
50 million people worldwide
Alzheimer’s disease – which affects approximately 50 million people worldwide – is predominant in people over the age of 65 (4 to 5% of cases of Alzheimer’s disease are found before the age of 65) . The medical treatments developed to date, to slow down and counter the degenerative process of Alzheimer’s disease, aim to prevent the formation of amyloid plaques forming between neurons, as well as tau protein aggregates.
The tau protein is present in the axons of neurons: it is associated with microtubules and acts by regulating their dynamics. Thus, the tau protein is linked to neurofibrillary degenerations occurring inside 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 made up of tubulin – involved in various functions importance, including intracellular transport, and cell division or mitosis).
Overactivated RAS (by SARS-CoV-2 or the vaccine spike protein), Covid-19 and Alzheimer’s disease: what is the link?
It has been observed (by clinicians and pathologists) cases of Alzheimer’s disease in people (including young adults), following a natural infection with SARS-CoV-2 (or even an anti-Covid-2 vaccination). 19) of these. As mentioned previously, a viral infection with SARS-CoV-2 (or even sometimes an anti-Covid-19 vaccination) causes dysfunction of the ARS, via an excess of the hormone angiotensin-2 (normally degraded by the receptor ACE2 -enzyme of conversion of angiotensin-2- to which the viral or vaccine spike protein binds) and the “deleterious” overactivation of the AT1R receptor (of the RAS), at the origin of Covid-19 diseases. The overactivated AT1R receptor is pro-hypertensive, that is, it induces high blood pressure. This has an impact on brain function.
Neurological disorders
Indeed, arterial hypertension is clearly identified as a major factor in mild or severe neurodegenerative disorders such as dementia and Alzheimer’s disease. RAS inhibitors (eg sartans, ACE inhibitors of angiotensin-1 converting enzyme) have been shown to have beneficial effects on neurodegenerative diseases and other cognitive dysfunctions (these beneficial effects are far superior to other types known hypertensives). Excess of the hormone angiotensin-2 is thus associated with neurological disorders, including deficit in the acquisition of spatial memory. These neurological disorders and alterations in cognitive functions are accompanied by an accumulation of beta-amyloid proteins in the cerebral cortex, as well as damage (decrease in synaptic content) of the perforating pathway of the hippocampus connected 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 vasoconstrictor effect of dysfunctional RAS
Thus angiotensin-2 (in excess in Covid-19) and the overactivation of RAS (responsible for Covid-19 diseases) promote the accumulation and deposition of beta-amyloid proteins (markers of Alzheimer’s disease), altering synaptic connections of brain cells and cognitive functions. In addition, the vasoconstrictor effect of dysfunctional RAS contributes to limiting blood flow in the brain, promoting neurovascular uncoupling, cerebral hypometabolism and the appearance of neurological damage.
How to limit/treat neurological (eg Alzheimer’s disease) and cardiovascular damage linked to RAS dysfunction?
The various molecules (quercetin, melatonin, thymoquinone, dexamethasone, sartans, ACE inhibitors, etc.) inhibiting the overactivation of the RAS are of interest, and in particular vitamin D which acts as a brake on the RAS, with beneficial effects – among others – on the incidence of neurodegenerative diseases, cognitive dysfunctions, and cerebrovascular accidents.
In conclusion, I describe here, for the first time, that there is a direct link between the dysfunctional renin-angiotensin or RAS system (because it is overactivated by the viral and possibly vaccinal spike protein) and the (potential) appearance of the neurodegenerative disease of Alzheimer’s in the host. And most certainly other degenerative diseases.
Covid: collection of censored articles by Jean-Marc Sabatier in English and Spanish
