This article by Prof. Jean-Marc Sabatier et al. is published
in the journal, Infectious Disorders - Drug Targets, 2023
BENTHAM SCIENCE PUBLISHERS
Renin-angiotensin
system, or RAS, is a physiological mechanism essential to human body function.
The SARS-CoV-2 virus causes overactivation and malfunction of this system. The
RAS regulates innate immunity, various microbiota, and the
autonomic processes of the kidney, lungs, and heart. The RAS is found in
every cell of every tissue and organ in the body, making it ubiquitous. The
excess of the hormone angiotensin-2, which overactivates the "deleterious"
RAS receptor AT1R, is directly accountable for the pathologies of Covid-19
caused by the malfunctioning. In fact, the AT1R receptor overactivated by
abundant angiotensin-2 has a variety of harmful effects on the human body by
inducing cellular signaling cascades. The AT1R receptor is pro-hypertensive as
it induces blood vessel constriction, pro-inflammatory since it causes a toxic
storm of pro-inflammatory cytokines, pro-oxidant because it increases the
production of reactive oxygen particles that kill cells, pro-thrombotic because
it promotes the formation of clots - or thrombi - that obstruct blood vessels,
and pro-angiogenic as it promotes the growth of blood vessels and tumors,
pro-hypoxemic because it reduces the load of red blood cells in oxygen and causes
desaturation of blood in oxygen, pro-hypoxic because it causes a deficit of
oxygen supply to various cells, tissues, and organs, pro-fibrotic because
it induces organ fibrosis, pro-hypertrophying because it increases organ
volume, and makes nitric oxide fall, affecting inflammatory, immune, and memory
phenomena.
Alzheimer's
disease is a form of dementia characterized by incapacitating neurological
diseases that affect the patient's behavior, memory, thinking, and reasoning
skills. Symptomatology usually develops gradually, but in the case of Covid-19
and long Covid it might occur unusually fast. Patients frequently experience
memory loss (amnesia), spatial-temporal disorientation, mood and personality
disturbances, reduced comprehension and/or inability to solve problems,
impairments of written and/or verbal expression (aphasia), and difficulties
managing daily tasks. Apraxia is the inability to perform motor movements
despite the existence of these "intact" functions, as well as
challenges with object recognition despite the existence of "intact"
sensory functions (agnosia).
Clinical
doctors and pathologists have noted the onset of Alzheimer's disease in a
variety of patients, including young adults, following a spontaneous infection
with the SARS-CoV-2 virus or even following immunization against Covid-19. A
viral infection with SARS-CoV-2 or even an anti-Covid-19 vaccination causes a
dysfunction of the RAS, via an excess of the hormone angiotensin-2 normally
degraded by the receptor ECA2 (angiotensin-2 converting enzyme) on 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, which means it provokes
arterial hypertension. This impacts the brain function. Evidently, arterial
hypertension has been identified as a significant risk factor for mild to
severe neurodegenerative disorders such as dementia and Alzheimer's disease.
RAS inhibitors, such as sartans and ACE inhibitors of angiotensin-1 converting
enzyme, have been equally shown to improve neurodegenerative diseases and other
cognitive dysfunctions. Thus, angiotensin-2, which is found in excess in
Covid-19 due to RAS overactivation, promotes the accumulation and deposition of
b-amyloid proteins (markers of Alzheimer's disease), impairing brain cell
synaptic connections and cognitive functions. Furthermore, the vasoconstrictive
effect of a dysfunctional RAS contributes to blood flow limitation in the brain,
promoting neurovascular uncoupling, cerebral hypometabolism, and the
development of neurological damage.
View the
article here: https://www.eurekaselect.com/article/132146
JOURNAL
Infectious Disorders - Drug Targets
DOI
10.2174/1871526523666230529162633
ARTICLE
TITLE
Covid-19 And Alzheimer's Disease: The Link Finally Established
ARTICLE
PUBLICATION DATE
29-May-2023
