Pyroptosis and cytokinemia in the CNS caused by SARS-COV-2 is a common aspect in neurodegenerative diseases. To think that diseases such as Alzheimer's, Parkinson's and Multiple and Amyotrophic Sclerosis, the latter in the SNP, can be elicited in this scenario, is, in my view possible. Obviously, since these diseases are chronic, the correlation will only be well defended in the medium and long term. In addition, other autoimmune diseases, such as type 1 diabetes, can also be eliminated, including in non-symptomatic children and adolescents. Therefore, I believe it is very pertinent that epidemiological studies that correlate these and other possible conditions in the post-contagion by SARS-COV-2 need to be started now.
Agree. Important issue to follow. Check out
Article COVID-19 and neurological disorders: are neurodegenerative o...
This is an important research since covid 19 is capable of crossing the BBB and cause neurodegeneration.
Who presented observations showing your statement to be justified, Michael Halim? Nikhil Kumar's link once more characterizes such claims as speculative ones.
Nasir Mustafa, wouldn't it make sense to check how the brain is actually changed in supposed instances of COVID-19 infections, on the one hand, and in particular so-called inflammatory or degenerative neurologic disorders on the other?
Then to rely on what proves distinctive of the given series of events?
The common point in neurodegenerative diseases is neuroinflammation. The role of the microglia, in specific profile M1, and lymphocytes T and B responses and, chemokine receptors are also involved in neuronal death and hence neurodegenerative diseases. Studies showed chemokines may induce neuronal death. Diseases as multiple sclerosis, Alzheimer's disease, Parkinson and cerebral ischemic disease. The study of SARS-CoV-2 damages in the central nervous system (CNS) is not only relevant for the moment, but in future can contributes for knowing phisiopatholgy of the neurodegenerative diseases, after viral process
Please, Noelio J. Menezes-Filho, are there any findings that allow to tell MS / Alzheimer's disease / Parkinson / cerebral ischemic disease or also SARS-CoV-2 related / traumatic/thermic/other CNS damages reliably apart ... simply on the basis of particular neuroinflammatory phenomena?
Will jumbling up different things under such broad umbrella terms as neurodegeneration or neuroinflammation contribute to elucidating their nature and cause?
Dear Fran Schelling, yes, this is a relationship that has already been well documented in the scientific literature. Numerous studies demonstrate that the common point between these neurodegenerative pathologies is neuroinflammation. The microglia's participation is already there. consensus. I even participated in studies that culminated in SCIENTIFIC articles in partnership with researchers from Spain (CSIC and NiCE-IMIB), Chile and Cuba that demonstrate the role of inflammation in vitro and in vivo models for Multiple Sclerosis and Parkinson. To mimic Parkinson's in vivo we use, for example, the pro-neurotoxin1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 6-OHDA and catechins. In the models to mimic Multiple Sclerosis, I used to elicit the immune model viral response (Theiler's virus) and Immunological elicitation using the basic myelin protein (MBP) and the proto-lipid protein (PLP), the latter, essentially immunological models. In all these studies and in a hundred others carried out around the world, the central finding is the role of the Immune response in the self-sustaining microenvironment of the CNS. With clear evidence of microglial activity, specifically in its M1 inflammatory profile. Inflammation is, already widely evidenced, a factor that promotes these diseases. In the Peripheral Nervous System, patients susceptible to developing Amyotrophic Lateral Sclerosis, whose main implication involves SOD have no aggravated condition in COVID-19. I hope I have contributed.
Dreadfully sorry, Noelio J. Menezes-Filho, never to have come across any shred of evidence showing any phenomenon of our inflammatory respectively immune response - be it to something set free from inside or outside the body, CNS, OR PNS - to either precede or at least be diagnostic, of any of the conditions ("defined" first by simply unexplained clinical disorders) in question.
No wonder there seems to be a consensus not to address any such question.
Sorry, i'm an immunologist and my doctorate was based on the immune response in multiple sclerosis and i know another reality. The number of studies involving this immune response is absurdly large. I really do not know this reality to which you report, I really do not. The evidence of involvement of the Immune system is such that these diseases are known to be autoimmune. Furthermore, as multi-causal and multifaceted diseases, assigning a single reason for them is a mistake. I believe that a search for articles, from the last 10 years, that reinforce my argument can bring you good answers.
Why not compare the immune responses seen in MS with those seen in conditions of a known origin?
Yes, Sure, everytime. Although the innitial phasis, ethiological factors and cronological aspects of the signals and symptoms and evolution are distinct, between themself inclusive.The Neurodegenerative diseases, as Multiple Sclerosis, Alzheimer's and Parkinson's, on the inflammatory induction pathways, has, in immunological response, commons mechanisms . So, as common aspect evolutionary, the neuroinflammation and imunne responses, in specific of the microglial response, showed promise as therapeutic strategy. And, today knowing that microglial profile M1 is responsable for sustainable of the microenvironment inflammatory, and that the retroactivity of the damages, promoted for inflammatory microglial activity, in the SNC, in MS specially, causes neuronal deads. Finding as we blocked this cycle, is necessary. However, this is the beginning of the begin.