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SourceL Neuro-COVID  Aug 10, 2020  3 years, 8 months, 2 days, 15 hours, 18 minutes ago

Neuro-COVID: University Of Michigan Academic Warns Of Potential Memory Loss And Dementia In COVID-19 Patients

Neuro-COVID: University Of Michigan Academic Warns Of Potential Memory Loss And Dementia In COVID-19 Patients
SourceL Neuro-COVID  Aug 10, 2020  3 years, 8 months, 2 days, 15 hours, 18 minutes ago
Neuro-COVID: Dr Natalie C. Tronson, an Associate Professor of Psychology from the University of Michigan in an article in The Conversation warns of potential memory loss and also the possible conditions of dementia as a result of the SARS-CoV-2 coronavirus effects on the brain.

Many patients suffering from COVID-19 exhibit neurological symptoms, from loss of smell, to delirium, to an increased risk of stroke. There are also longer-lasting consequences for the brain, including myalgic encephalomyelitis /chronic fatigue syndrome and Guillain-Barre syndrome.
Some of these effects may be caused by direct viral infection of brain tissues or as growing evidence suggests, additional indirect actions triggered via the virus’s infection of epithelial cells and the cardiovascular system, or through the immune system and inflammation, contribute to lasting neurological changes after COVID-19. and
Dr Tronson who specializes in the the role of immune cells in the brain and how memory is persistently disrupted after illness and immune activation was concerned  if there will be a COVID-19-related wave of memory deficits, cognitive decline and dementia cases in the future.
Accordingly, many of the symptoms we attribute to an infection are really due to the protective responses of the immune system. A runny nose during a cold is not a direct effect of the virus, but a result of the immune system’s response to the cold virus. This is also true when it comes to feeling sick. The general malaise, tiredness, fever and social withdrawal are caused by activation of specialized immune cells in the brain, called neuroimmune cells, and signals in the brain.
Dr Tronson says that although these changes in brain and behavior, annoying for our everyday lives, are highly adaptive and immensely beneficial. By resting, one allows the energy-demanding immune response to do its thing. A fever makes the body less hospitable to viruses and increases the efficiency of the immune system. Social withdrawal may help decrease spread of the virus.
Besides changing behavior and regulating physiological responses during illness, the specialized immune system in the brain also plays a number of other roles
Recently it was discovered that the neuroimmune cells that sit at the connections between brain cells (synapses), which provide energy and minute quantiti es of inflammatory signals, are essential for normal memory formation. . and and and
However unfortunately, this also provides a way in which illnesses like COVID-19 can cause both acute neurological symptoms and long-lasting issues in the brain.
It has been observed that during illness and inflammation, the specialized immune cells in the brain become activated, spewing vast quantities of inflammatory signals, and modifying how they communicate with neurons. For one type of cell, microglia, this means changing shape, withdrawing the spindly arms and becoming blobby, mobile cells that envelop potential pathogens or cell debris in their path. But, in doing so, they also destroy and eat the neuronal connections that are so important for memory storage. and
A unique type of neuroimmune cell called an astrocyte, typically wraps around the connection between neurons during illness-evoked activation and dumps inflammatory signals on these junctions, effectively preventing the changes in connections between neurons that store memories.
As a result of  COVID-19 involving a massive release of inflammatory signals, the impact of this disease on memory is particularly of concern. That is because there are both short-term effects on cognition (delirium), and the potential for long-lasting changes in memory, attention and cognition. There is also an increased risk for cognitive decline and dementia, including Alzheimer’s disease, during aging.
Dr Tronson answer the question that if activation of neuroimmune cells is limited to the duration of the illness, then how can inflammation cause long-lasting memory deficits or increase the risk of cognitive decline?
According to her, both the brain and the immune system have specifically evolved to change as a consequence of experience, in order to neutralize danger and maximize survival. In the brain, changes in connections between neurons allows us to store memories and rapidly change behavior to escape threat, or seek food or social opportunities. The immune system has evolved to fine-tune the inflammatory response and antibody production against previously encountered pathogens.
However at the same time long-lasting changes in the brain after illness are also closely linked to increased risk for age-related cognitive decline and Alzheimer’s disease. The disruptive and destructive actions of neuroimmune cells and inflammatory signaling can permanently impair memory. This can occur through permanent damage to the neuronal connections or neurons themselves and also via more subtle changes in how neurons function. and
The connection between COVID-19 and persistent effects on memory are based on observations of other illnesses. For example, many patients who recover from heart attack or bypass surgery report lasting cognitive deficits that become exaggerated during aging.
Interestingly another major illness with similar cognitive complications is sepsis- a multi-organ dysfunction triggered by inflammation.
It has been observed in animal models of these diseases that impairments of memory, and changes in neuroimmune and neuronal function that persist weeks and months after illness.
Currently even mild inflammations, including chronic stress, are recognized as risk factors for dementias and cognitive decline during aging.
Dr Tronson says that even in her own laboratory, her study teams have also observed that even without bacterial or viral infection, triggering inflammatory signaling over a short-term period results in long-lasting changes in neuronal function in memory-related brain regions and memory impairments. and