What are the latest updates about the route of transmission and its impact?
Dear Dr. Ebada,
We know very little about COVID-19 at this moment and its effects on the developing and/or mature brain. In general viral infections can impair charnolophagy (CB autophagy) which is the basic molecular mechanism of intra-cellular detoxification (ICD) for normal function to remain healthy. By attacking the most sensitive neural progenitor cells in the brain, the virus can alter their pluripotency and induce charnolosome (CS) destabilization implicated in inflammasome (particularly NRLP-3) activation to induce hypercytokinemia and charnoptosis (CB apoptosis) implicated in pyroptosis, apoptosis, and necrosis of sensitive hippocampal and other CNS neurons by releasing Panx-1, Viroporine, and gasdermins to cause Charnoly Body Molecular Pathogenesis (CBMP) implicated in early morbidity and mortality through its general (Viral) lytic cycle.
For more details, you may please refer to my books " The Zika Virus Disease: Prevention and Cure" The Charnoly Body: A Novel Biomarker of Mitochondrial Bioenergetics" Fetal Alcohol Spectrum Disorder; and Nicotinism and Emerging Role of E-Cigarettes. I wish I could write more about it.
Dr. Ebada, It is all about Environmental Sanitation, our own Life-Style, Immunity, Mitochondrial Bio-energetics and intracellular detoxification through charnolophagy (CB autophagy), which is compromised by COVID-19 through CS destabilization to cause early morbidity and mortality by infecting the CNS. Thanks.
With Warm regards,
Sushil Sharma, Ph.D; D.M.R.I.T
Academic Dean
American International School of Medicine
Guyana, South America
.
https://www.medscape.com/viewarticle/928903
COVID-19 thought to affect the brain in 4 ways:
1) direct viral injury of nervous tissue, such as occurs with herpes simplex encephalitis; 2) an excessive immune response in the form of a "cytokine storm."; 3) unintended host immune response effects after an acute infection.; 4) indirect viral injury results from the effects of systemic illness.
Hello DR EBADA: Yes, COVID-19 affects the CNS, resulting in fits and seizures and other neurological imbalances--for details please peruse the following links:
https://gulfnews.com/world/asia/coronavirus-how-does-covid-19-affect-the-brain-1.1587181395470
https://www.wired.com/story/what-does-covid-19-do-to-your-brain/
Regards--
Any disease that affects humans affects the rest of its organs
Doctors at Henry Ford tested the woman for Covid-19, and she came back positive. They also ordered CT and MRI scans. The images showed a brain aflame, its folds swelling against the patient’s skull. On the computer screen, white lesions dotted the gray cross-sectioned landscape—each one filled with dead and dying neurons in regions that normally relay sensory signals, regulate alertness, and access memories. On the screen they appeared white. But in the electrical grid of the patient’s brain, those areas had gone dark.
Mahmoud Ahmed Ebada following article will be helpful for you.
Article Evidence of the COVID-19 Virus Targeting the CNS: Tissue Dis...
Dear Dr. Ebada,
We know very little about COVID-19 at this moment and its effects on the developing and/or mature brain. In general viral infections can impair charnolophagy (CB autophagy) which is the basic molecular mechanism of intra-cellular detoxification (ICD) for normal function to remain healthy. By attacking the most sensitive neural progenitor cells in the brain, the virus can alter their pluripotency and induce charnolosome (CS) destabilization implicated in inflammasome (particularly NRLP-3) activation to induce hypercytokinemia and charnoptosis (CB apoptosis) implicated in pyroptosis, apoptosis, and necrosis of sensitive hippocampal and other CNS neurons by releasing Panx-1, Viroporine, and gasdermins to cause Charnoly Body Molecular Pathogenesis (CBMP) implicated in early morbidity and mortality through its general (Viral) lytic cycle.
For more details, you may please refer to my books " The Zika Virus Disease: Prevention and Cure" The Charnoly Body: A Novel Biomarker of Mitochondrial Bioenergetics" Fetal Alcohol Spectrum Disorder; and Nicotinism and Emerging Role of E-Cigarettes. I wish I could write more about it.
Dr. Ebada, It is all about Environmental Sanitation, our own Life-Style, Immunity, Mitochondrial Bio-energetics and intracellular detoxification through charnolophagy (CB autophagy), which is compromised by COVID-19 through CS destabilization to cause early morbidity and mortality by infecting the CNS. Thanks.
With Warm regards,
Sushil Sharma, Ph.D; D.M.R.I.T
Academic Dean
American International School of Medicine
Guyana, South America
.
The most common neurological
manifestations in covid are dizziness, headache, and encephalopathy. The most
common peripheral signs and symptoms were anosmia, dysgeusia and muscle
injury. Stroke complicated COVID-19 infection in 5.9% of patients at median 10 days after symptom onset.
Many viral diseases cause of encephalitis and is responsible for high rates of morbidity, many with permanent neurologic sequelae. Moreover, depending to the virus, high mortality rates. Many viral etiologies agents as herpesviruses (HSV‐1 and HSV‐2), non‐polio enterovirus, and arboviroses as dengue, Zika, and chikungunya showed brain tropism. In addition, many neurodegenerative diseases has correlation with the neuroinflammation promoved for immunological response against viral agents. However, us knows very less that us need. Many studies showed that Coronavirus, for example, can attacks the CNS, but yet is very precocious for affirmations or, inferences. Today, us knows that has that studies.
On a similar thread on neurology and COVID-19, a scientific article is cited in which, among other neurological symptoms, schizophrenia is mentioned as being caused by a patient's contraction of the COVID-19 virus.
Thanks for your wonderful educative submissions Covid 19 have on human health.
...noted that studies of another member of the coronavirus family, SARS-CoV, indicate that direct brain entry is possible, and direct coronavirus spread to the medullary cardiorespiratory center may partially underlie COVID-19 respiratory failure. SARS-CoV nucleic acid has been found in the cerebrospinal fluid and brain tissue of patients infected with SARS-CoV, while invasion of the brain with SARS-CoV via the olfactory system in mice can also occur.
https://www.medscape.com/viewarticle/928903
Findings indicate that SARS-CoV can enter the human nervous system with evidence from both postmortem brains and detection in cerebrospinal fluid of infected individuals. Here we consider the ability of SARS-CoV2 to enter and infect the human nervous system based on the strong expression of the ACE2 target throughout the brain.
http://molpharm.aspetjournals.org/content/early/2020/04/01/molpharm.120.000014
COVID-19 may affect the nervous system via four potential mechanisms, which may overlap. The first is direct viral injury of nervous tissue, such as occurs with herpes simplex encephalitis. Although there are some suggestive case reports, there is no definite proof that the SARS-CoV-2 virus directly damages the central nervous system (CNS).
https://www.medscape.com/viewarticle/928903
The second type of injury results from an excessive immune response in the form of a "cytokine storm." Cytokines can cross the blood-brain barrier and are associated with acute necrotizing encephalopathy. Only one case concurrent with COVID-19 has been reported.
https://www.medscape.com/viewarticle/928903
The third mechanism of nervous tissue damage results from unintended host immune response effects after an acute infection. An example of this type of indirect CNS injury is Guillain-Barré syndrome (GBS). One case of GBS associated with COVID-19 has been reported, but the evidence for cause and effect is weak.
https://www.medscape.com/viewarticle/928903
The fourth mechanism of indirect viral injury results from the effects of systemic illness. Neurologists are accustomed to seeing severely ill patients in the intensive care unit develop neurologic symptoms such as encephalopathy, critical illness myopathy, and neuropathy. Most cases of COVID-19-related neurologic complications appear to fall into this category.
https://www.medscape.com/viewarticle/928903
Has anyone found an opportunity to do cranial MRIs, even longitudinal studies on COVID-19 patients?
Dear Mahmoud,
As the number of Corona virus cases and reports and publications increasing, we are starting to see an increasing number of reports of neurological symptoms, perhaps in over a third of patients. Many of these symptoms were mild and include things like headaches or dizziness that could be caused by a robust immune response. Other more specific and severe symptoms were also seen and include loss of smell or taste, muscle weakness, stroke, seizure, and hallucinations.
Several recent studies have identified the presence of neurological symptoms in COVID-19 cases. Some of these studies are case reports where symptoms are observed in individuals. Several reports have described Covid-19 patients suffering from Guillain–Barré syndrome. Guillain–Barré syndrome is a neurological disorder where the immune system responds to an infection and ends up mistakenly attacking nerve cells, resulting in muscle weakness and eventually paralysis.
Other case studies have described severe Covid-19 encephalitis (brain inflammation and swelling) and stroke in healthy young people with otherwise mild Covid-19 symptoms.
Changes in consciousness, such as disorientation, inattention, and movement disorders, were also seen in severe cases and found to persist after recovery.
SARS-CoV-2, the coronavirus that causes Covid-19, may cause neurological disorders by directly infecting the brain or as a result of the strong activation of the immune system.
Recent studies have found the novel coronavirus in the brains of fatal cases of Covid-19. It has also been suggested that infection of olfactory neurons in the nose may enable the virus to spread from the respiratory tract to the brain.
Cells in the human brain express the ACE2 protein on their surface. ACE2 is a protein involved in blood pressure regulation and is the receptor the virus uses to enter and infect cells. ACE2 is also found on endothelial cells that line blood vessels. Infection of endothelial cells may allow the virus to pass from the respiratory tract to the blood and then across the blood-brain barrier into the brain. Once in the brain, replication of the virus may cause neurological disorders.
SARS-CoV-2 infection also results in a very strong response by the immune system. This immune response may directly cause neurological disorders in the form of Guillain–Barré syndrome. But brain inflammation might also indirectly cause neurological damage, such as through brain swelling. And it’s associated with – though doesn’t necessarily cause – neurodegenerative diseases such as Alzheimer’s, Parkinson’s and amyotrophic lateral sclerosis (ALS, motoneuron disease). ALS patients may be particularly vulnerable to Covid-19, as their respiratory neuromotor system is already directly affected and weakened by the disease. Recently an ALS patient in England died soon after diagnosed with Covid-19.
Therefore, effects of SARS-CoV-2 on the brain may be an interactive process with already existing conditions.
Best wishes,
Refik Kanjhan
Respected Dr. Kanjhan,
Yes indeed ! The signs and symptoms you mentioned above are all described in greater detail in my books on "Zika Virus Disease: Prevention and Cure" and The Charnoly Body: A Novel Biomarker of Mitochondrial Bioenergetics".
It seems, there is considerable immunopathological similarities in the basic molecular mechanism of action particularly when the virus interacts with our neural progenitor cells, derived from induced pluripotent stem cells.
Currently, our macrophage-charnolophagy (CB-autophagy) system is not experienced enough to eradicate them efficiently particularly in a pediatric and aging immuno-compromised population with pre-existing conditions to sustain intra-cellular detoxification and mitochondrial quality control for normal cellular function to remain healthy. This can be achieved by developing novel charnolpharmacotherapeutics and/or vaccines for their prophylaxis.
The charnolosome index (charnolosome/inflammasome) determines the patient's prognosis in response to treatment or without treatment, in addition to our own life style ( diet preference, exercise, sex, sleep, and environmental sanitation).
It is interesting to share with you that generally animal viruses infect animals (we are also animals). Generally, plant viruses are not known to cause human illnesses perhaps because of diverse amino acid and nucleic sequences. (Please correct me if I am wrong)
I hope we will have soon a better answer to combat this and other microbial infections.
Respectfully submitted,
Sushil Sharma, Ph. D; D.M.R.I.T
Academic Dean
American International School of Medicine
Georgetown, Guyana, South America
Loss of smell and taste is a early symptoms of Covid-19 due to SARS Cov-2 reached into brain by cranial nerve 1 and 2.
It affects him negatively by thinking about the negative aspects surrounding him.
Curiously, in none of the more than 150 autopsies done on COVID 19 patients, direct viral affections of nervous structures seem to have come to the fore.
Are there different reports?
The virus can affect the brain in several ways but mainly by intravascular routes
What about the affinity of particular viruses to particular cellular formations inside and outside the brain, Luis Rodrigo: Aware of comparable observations made in COVID 19 autopsies?
COVID-19 symptoms vary widely regardless of demographics and vital statistics. Some, but certainly not all, patients show signs of dementia, those who are elderly, but also others who are not.
Sorry for not having made my point sufficiently clear, Nancy Ann Watanabe.
COVID-19 autopsies seem to have shown remarkably frequent venous/vascular circulatory problems, no virus affinity to particular neuronal elements such as seen in the Spanish flu or polio.
Dear Dr Ahmed: The COVID-19 infection may lead to a dangerous condition called acute necrotizing hemorrhagic encephalopathy, or ANE, It’s a rare complication known to occasionally accompany influenza and other viral infections, though usually in children. With the flu, scientists believe such brain damage is caused not so much by the virus itself but by squalls of inflammation-inducing molecules called cytokines, which are sometimes produced in excess by the body’s immune system during an infection. Scientists are still trying to figure out if the same is true for Covid-19, or if the coronavirus called SARS-CoV-2 is actually invading the nervous system directly. It’s an open question, the answer to which could have wide-ranging implications for how doctors diagnose and treat Covid-19 patients. Regards-
Dear Dr. Durrani: Do you have concrete pieces of evidence on the frequency of ANE, or also the less aggressive ADEM, in COVID-19 patients?
Dear Dr Franz: Here you are Sir:
https://www.wired.com/story/what-does-covid-19-do-to-your-brain/
Thank's Dr. Durrani - It's a pity the links doesn't offer the pictorial evidence I am looking for.
I think coronaviruses might affect the brain and disrupt the BBB, this nano-scaled virus might cause clots in the brain as this virus could alter the blood components and result in blood clottings
Article A first Case of Meningitis/Encephalitis associated with SARS...
How does COVID-19 infection affect the brain?
I consider that COVID - 19 affects the brain by different mechanisms: social isolation; stress due to the possibility of contracting the disease to people, family members and loved ones from all over the world; encephalitic and encephalitis by the virus itself, described in several scientific articles.
Thank's for showing these brain slices of a recent SARS virus encephalitis, Dr. Rufai, illustrating the complex interrelationships between clinical indications of a bulbar or global brain affection and a one-sided temporobasal focus of inflammation.
Wouldn't embark on the hardly ever to be comprehensively dealt with complexities of additional psycho-social interfering factors turned things unavoidable speculative, Dr. Rodriguez?
During 2002-2003, cases of patients with polyneuropathy, ischemic cerebrovascular disease, and encephalitis associated with the SARS-CoV-1 virus were described, an idea supported by evidence of cerebral edema and meningeal vasodilation in autopsies of patients who died of the infection. Studies in murine models also showed viral particles and SARS-CoV-1 genomic sequences in brain neurons, for which an infection route was proposed through the olfactory epithelium and the olfactory bulb to the brain, a hypothesis that has also been raised for explain the neurological compromise of SARS-CoV-2, since in neurons and glial cells there is a high expression of angiotensin-converting enzyme 2 (ACE-2) receptors.
Lung infections with different human coronaviruses have been observed to cause an increase in alveolar and interstitial inflammatory exudate, which generates a state of hypoxia that induces anaerobic metabolism. Likewise, a severe hyperinflammatory systemic reaction occurs characterized by an excessive release of proinflammatory factors such as interleukin (IL) 6, IL 12, IL 15 and tumor necrosis factor alpha, which is called a cytokine storm that seems to be common to several of the coronaviruses, especially SARS-CoV-2. Furthermore, studies in in vitro cell cultures identified that glial cells, after being infected by different coronaviruses, express an increase in the secretion of these proinflammatory substances. This hyperinflammatory syndrome at the CNS level could cause chronic inflammation and brain damage.
This description, as well as the main neurological manifestations described to date, we detail in our letter to the editor available at the following link.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7211628/
Won't other colleagues, like me, feel overwhelmed in being confronted with so many different pathological states, affecting different domains of either macro- or microsphere in such a concentrated form, Dr. Sánchez-Duque?
Article Neuropathogenesis and Neurologic Manifestations of the Coron...
Here is a recent review published in JAMA discussing the proposed mechanisms of invasion and the neurological manifestations.
There are several ways such as the direct invasion, the associated inflammation and the intravascular coagulation as main mechanisms
There are many effects described in the following article:
https://www.medscape.com/viewarticle/928903
Reminding the neurological community of all these potential lines of Corona-Virus research awaiting their being explored might be well worth the effort, Drs. Elsayed and Rodrigo.
Follow This Link Please:
https://www.omicsonline.org/scientific-journals.php
If you are interested in COVID and the effects on the brain please see
https://rax.rochester.edu/s/1676/rd16/interior.aspx?sid=1676&gid=2&pgid=6800&cid=10310&ecid=10310&crid=0&calpgid=13&calcid=664
This is an on-line set of lectures. The lecturers will also be open for email questions.
the precise mechanism how Covid 19 affect the brain is not completely clear but we think there three different ways where the virus enters the brain
first through the olfactory system and possible spread through the post synaptic pathway and may causes encephalitis
the second possible way is through the infected blood cells like macrophages and others WBC which enters the brain through the blood brain barrier(BBB) and cause diffuse central nervous system infections and possible endothelial blood vessel with subsequent vasculitis like picture.
the third possibility is through what calls is cytokine storms which result of severe body infection. encephalitis, ischemic stroke as well as hemorrhagic strokes have been reported in in Covid 19 admitted patient in fact we had a young lady patient who presented with large MCA stroke and confirmed positive covid-19
Aren't the central nervous effects of COVID 19 infections as non-specific as the supposed autoimmune activities ascribed to multiple sclerosis?
Aren't we here going to enter another vicious circle?
Ought not to be shown in which part(s) of the brain these viruses settle down respectively become deleterious ... and why with so widely differing delays?
The same 'may be's' and 'don't know's' - don't they keep up reiterating in virtually all COVID 19 respects?
Nervous and pressure are the cause of it, which affect our brain.
What here nervous? what kind of pressure is at work here, Dr. Gomeseria?
Dear DR Mahmoud: Some scientists suspect that Covid-19 causes respiratory failure and death not through damage to the lungs, but the brain – and other symptoms include headaches, strokes and seizures.
https://www.bbc.com/future/article/20200622-the-long-term-effects-of-covid-19-infection
https://www.hopkinsmedicine.org/health/conditions-and-diseases/coronavirus/how-does-coronavirus-affect-the-brain
https://www.bbc.com/news/health-53081022
Kind regards--
Thank you for making this point, DR Ijaz Durrani - supported by MRI studies showing that Covid 19 fatalities by vascular lesions are five times as frequent as pulmonary ones.
Now, more than 300 studies from around the world have found a prevalence of neurological abnormalities in Covid-19 patients, including mild symptoms like headaches, loss of smell (anosmia) and tingling sensations (arcoparasthesia), up to more severe outcomes such as aphasia (inability to speak), strokes and seizures.
https://www.bbc.com/future/article/20200622-the-long-term-effects-of-covid-19-infection#:~:text=Now%2C%20more%20than%20300%20studies,speak)%2C%20strokes%20and%20seizures.
https://www.hopkinsmedicine.org/health/conditions-and-diseases/coronavirus/how-does-coronavirus-affect-the-brain
https://www.sciencemag.org/news/2020/07/brain-fog-heart-damage-covid-19-s-lingering-problems-alarm-scientists
Why is so little told about how the Covid-19 patients' neurological abnormalities come about, Dr. Durrani?
DR Franz Schelling: For your perusal , Sir!!
https://www.hopkinsmedicine.org/health/conditions-and-diseases/coronavirus/how-does-coronavirus-affect-the-brain#:~:text=Patients%20with%20COVID%2D19%20are,neurological%20issues%20due%20to%20strokes.
https://www.arabnews.com/node/1717621/world
https://www.wired.com/story/what-does-covid-19-do-to-your-brain/
https://theconversation.com/how-coronavirus-affects-the-brain-141100
There are many controversies about that. In any case it can occur in very few cases fortunately
DR Ijaz Durrani,
Telling link indeed ... please understand my difficulties to reconcile myself with the shown state of affairs
Some people who become ill with the coronavirus develop neurological symptoms. Scientists are struggling to understand why.
https://www.nature.com/articles/d41586-020-02599-5
Aren't serial MRIs that take advantage of recent advances (achieved largely by Mark Haacke) ideal for finding out why neurological symptoms develop?
How far such can be traced back to SARS-CoV-2, or to any more trivial, above all vascular, or to widely neglected venous causes?
I believe that the immunological response in inflammatory environment CNS is responsable. In special the immunological response of the microglia, specific profile M1. In many pacients, the immunological response against the SARS-CoV-2 promotes pyroptosis and hipercytokinemia due to a highly stimulated but ineffective immune system. This scenario promotes neurological symptoms and, also, promotes autoimmune diseases.
It was great to learn what this belief is grounded in, Dr. Menezes-Filho.
Have you any data showing the given biological responses actually differ from what is required to remove irreparably damaged own material? That they differ from what is seen to follow comparable destruction of a known origin? Or that they even precede the lesions which they are supposed to account for?
Yes, many scientific articles has showed, cells, as Microglia, in response to specific stimuli and/or Neuroinflammation, can to damage and kill neurons. This is fact in disease as Alzheimer’s, Parkinson’s, Huntington’s, and prion diseases, multiple sclerosis, amyotrophic lateral sclerosis, dementias, and etc. Moreover, many studies yet showed correlation, between of the role of Neuroinflammation in local microenvironment and prognostic the disease in this conditions. That is, this studies show that where microglia in your inflammatory profile are in, your the close interaction with neurons, astrocytes and oligodendrocytes, in the different regions, the inflammation is self-supporting. This results in the dysregulation of the defense function and cycles of the Neuroinflammation. Many pathways yet remain unknowing, sure. But, the physiologic role of the immune cells in neuronal dead is fact. Many by damage associated injury without immune cells, others for exacerbate action immunological, that's include error in several sensing and housekeeping physiological pathways knows. The new strategies searching acts in immune checkpoints to keep the microglial inflammatory response under control, this is fact. However, The Initiation or exacerbation of neurodegeneration damages, specially, in microglial functions may be a potential target therapy, if controlled. In case of the COVID-19, the point is: the pyroptosis and hipercytokynemia promoted, that maybe might have an impact in the progression of neurodegenerative disorders? This is my uncertainty.
Aren't there further uncertainties in discriminating the microglia/immune responses/neuroinflammation in Alzheimer's, Parkinson's, Huntington's, and all the other clinically defined unexplained diseases from those reflecting normal scavenging functions after neurotrauma, (white or red) cerebral infarction, or even cerebrospinal infections? be this either in their time course or their nature?
Of course yes, no have one explication unique, no have one cause unique for any disease is neurodegenerative. The multiple causes for Alzheimer (beta amyloid or alpha synuclein) and the pathophysiological process with Neuroinflammation e/or abnormal microglia activation and, others factors, is regardless of etiology. In this case, has an subsequently oxidative stress with sustained neuronal distress and, consequently neuronal death. This is fact. In Parkinson disease with dementia, for example, has as common point an excessive and pathological loss of neurons. This is fact. This is characterized for Neuroinflammation, whose principal mediators and actors are immune cells. Especially, brain-resident macrophages, the microglia. This immune cells are active and, pro-inflammatory microglia (M1 profile) are closely associated with protein aggregate pathologies characteristic of most dementias. Note this occurs, also, without physical trauma present. Moreover, many studies showed the many viral as triggers for Neuroinflammation and, consequently neurodegenerative processes, I repeat, without physical trauma. But, only pathogenic agents releasing cytotoxic mediators, active the microglia and others immune cells, as lymphocytes B, lymphocytes T cytotoxic and, macrophages. This is fact, for example, with LPS models or Theiler´s virus, in Vivo or in Vitro. Many, many studies showed in immunohistochemistry and flow cytometry analysis, that the phenotype of microglia (M1) type-dominant. And, therapeutic agents anti-inflammatory act for disbalance with microglial M2 profile overlapping against M1 profile. With decreased neuronal death and, with maintained homeostasis, parenchyma self-restore and, reacts to damage and pathogen-associated stimuli (DAMPS). In trauma cases anti-inflammatory strategies, although auto limited, initial working. This is depends for trauma extenze. But, in both cases, the immune cells role is clear, specific cells networks is most strongly correlated to neuropathology and, others strongly correlated to regression or slower progression of the disease. Thus far, this is known.
1- From brain fog to heart damage:
https://www.sciencemag.org/news/2020/07/brain-fog-heart-damage-covid-19-s-lingering-problems-alarm-scientists
2- Delirium:
https://covid.joinzoe.com/post/covid-brain-delirium
3-https://theconversation.com/how-coronavirus-affects-the-brain-141100
What I'd like to know, Dr. Menezes-Filho, is how to discriminate the scavenging function of biochemical and immune agents observed in boxer brains from the supposedly spontaneous biochemical and immune response attacks in all the spontaneous nervous and mental diseases being attributed to the latter.
I failed to learn this for beyond fifty years.
I understand. This is a dilema and very complex. However, trauma, virus, bacteria and, others agents act as triggers, although for different pathways, that'll on, in microenvironment of the CNS, inflammation and, oxidative stress. The common points of all neurodegerative diseases and actives immunological response. In the Multiple Sclerosis, for example, in many cases, the cycle of the desmyelization and remyelinization, initialized for different reasons, promotes neuronal damage and, microglia activation induced neuronal death, subsequently. In substantia nigra pars compacta, dopaminergic neurons are affected for traumatic event and non traumatic events, in both cases, also, common point, oxidative stress, neuronal death, initilized Parkinson disease. In this scenario, inflammatory and oxidative stress, the microglia is actived and, the disbalance between profiles M1 (inflammatory) and M2 ( anti-inflammatory) the prognostic follows. For Us the point is? Controlled microglial disbalance, we controller the prognostic? Thus, for Us, the causes not searchingly for this reason.
A review of the 3 stages of brain damage caused by covid-19 infection:
https://www.medscape.com/viewarticle/933131
But how, Dr. Menezes-Filho, do you think are your observations to be reconciled with the ways in which multiple sclerosis (and amyotrophic lateral sclerosis) were originally quite indubitably identified - as was first pointed out by me in 1982 and was exposed to anyone's critique 20 years later (see www.ms-info.net)?
What amazes me the most is the missing differentiation of brain and cord MS.
Dear Dr. Durrani, who actually showed Coronaviruses to invade neurons, and such neuronal infections to have become clinically manifest?
All I could get hold of is evidence of early or delayed MRI-findings of scattered multifocal brain lesions related to PCR tests developed to trace SARS-CoV-2 infections ... which could not be discriminated from hypertensive brain lesions.
Dear professor Franz, this is face of science. For example, today, we believe that multiple sclerosis (MS) is a inflammatory disease, chronic disease inflammatory. With target of the central nervous system, involving demyelination and axonal degeneration. Today, we believe, tomorrow maybe not. Many, substantial progress, has been obtain. New drugs development, new approaches defined. But, in MS relapsing–remitting, for example, treatment of the progressive forms of the disease remains unsatisfactory. The complexity pathophysiological mechanisms involved in MS progression as the chronic inflammation, with activation of microglia and, others cells as T cells and B cells, is a goal pathophysiological feature. The Inflammation environment can promotes mitochondrial damage in neurons, oligodendrocytes and, astrocytes with energy deficit. This deficit, can, in neurons, promotes axonal damage with irreversible neuronal damage or reversible damage, but in microglia cell act as signal for phagocytosis induces. In Oligodendrocytes, can act as inhibitor of the myelin synthesis. For Astrocytes the mitochondrial damage, can disbalance in glucose levels with, subsequent, oxidative species synthesis. In the three cases, inhibitors efects occur, efects that cannot protect axons from degeneration, but, otherwise neurodegeneration accelerated in demyelinated neurons. In Amyotrophic Sclerosis, in special, in cases of the SOD1 deficiency (mutstion), the complexity as is inhibitors of the homestasis act. Clear, somes we knowing, specially the that inflammatory and oxidative stress factors. However, science is frenetic stimulus for discords and, concordances. We think that natural compounds as alkaloids, terpenes and flavonoids can act as pharmaceutical, especially for anti-inflammatory and anti-oxidatives, keeping conditions for repair self-mechanism. In many cases, terpenes, as Cannabidiol, inhibitor the microglial profile Mi (inflammatory) and, stimulate anti-inflammatory profile M2. Others studies use Flavonoids as rutin and quercetin. Results are obtained, some promise. However, the must important, learning how mechanisms physiopathology initial and act. Where are your progression points, if are reversible, where not, etc.
Dear Dr Franz Schelling: I hope this is the germane link you're look for :
Article Nervous system involvement after infection with COVID-19 and...
Please take a look at the following useful link:
https://www.livescience.com/brain-invasion-coronavirus.html
Thank you for the second link, in particular, Dr. Durrani!
Do you know how and where the virus was identified in its autopsy brains?
Or how to get access to the second paper as a whole (I could only ask for the paper to the link you sent first)?
Great Noelio, your "Today, we believe, tomorrow maybe not."
But why not check whether we rightly believe certain (or all) SARS-CoV-2 positive
PCR-tests detect this kind of coronavirus? Why not disprove repeated claims such tests proved positive on some kind of not only goats but even fruits?
As for MS: Why not check whether disparate isolated neuronal dysfunctions scattered with certain timings actually reflect a special kind of demyelination?
Dear Dr Franz Schelling: Here is what I have ferreted out concerning your last question:
https://www.youtube.com/watch?v=NQ0FaaJ73xc
What autopsies reveal concerning brain, heart and lung:
https://www.washingtonpost.com/health/2020/07/01/coronavirus-autopsies-findings/
Hope it helps!
Take a look at the following link:
https://www.downtoearth.org.in/blog/health/how-covid-19-affects-the-brain-72190
Dr Franz Schelling, science and absolute truth don't combine. In my questions, I find answers, possible answer now, comparative with renomed studies and, that has others pathogens as refree. In this studies, correlation showed that neuroinflammation and, ocidative stress with microglial activation as indissolubles steps to pathology progress. In MS case, in many cases, the lesions are secondary the neuronal death for pathologic acts microglial. This cell not the unique guilty, but your activation in inflammatory profile (M2), self-starter the cycle of the remyelinization and demyelination, coming post-inflammatory stresses (Inflammation is present in all subsets of MS) exhausting the mechanisms repair and neuronal death, as result. The sclera present in MRI not measure this. The point is SARS-COV-2 can promotes the necessary microenvironment ( inflammatory and oxidative) for this? When we will knowing? As can we wil know? Suggestion: epidemiological studies, this us point.
What sense makes the results of any scientific endeavor, any knowledge, if we can't rely on it? if science is no longer striving for absolute truth?
It's a pity, Dr. Durrani, the data of your links are hard to reconcile with what far larger autopsy-series done in Germany and Italy, but also in vivo MRIs of COVID-19 cases have shown.
Who can here be relied upon?
Article Letter by Rajendram et al Regarding Article, “Clinical Chara...
This article may be relevant.
Rajkumar Rajendram yet we need investigate more, but the damages in CNS, promotes for SARS-COV-2 is fact, the science community showing in many studies as is possible, in future, have many cases of the neurodegerative diseases pos-COVID-19. Best, COVID-19 will promotes, in special, through the neuroinflammation and, hypercytokinemia. Remember also, diabetes type I in children and teenagers, is possible.
Rajkumar Rajendram: How can your letter be said to reduce the insecurity about the nature of the positive SARS-CoV-2 PCR tests' relationship to any topical autopsy findings?
The list now includes stroke, brain haemorrhage and memory loss. It is not unheard of for serious diseases to cause such effects, but the scale of the COVID-19 pandemic means that thousands or even tens of thousands of people could already have these symptoms, and some might be facing lifelong problems as a result. Please take a look at the following useful link:
https://www.nature.com/articles/d41586-020-02599-5#:~:text=The%20list%20now%20includes%20stroke,lifelong%20problems%20as%20a%20result.
It is important for science that we exhaust all hypotheses. However, there is no longer any controversy about how the virus can act, for example, on the CNS. Hypercytokinaemia and inflammation are more than the necessary evidence to understand how DAMPs, which we have known for a long time, can promote neurodegenerative diseases. We now need to discuss how to avoid them. Other systems may suffer from the damage, children and adolescents may have type 1 diabetes.
Aren't we going to be, someday, exhausted by all the hypotheses that zoom in on clinical, histological, biochemical, or pathological findings being common to countless etio-pathogenetically different conditions? On findings that haven't been properly evaluated for their uniqueness, their specificity?
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