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.  Neuroimmune cells sit at synapses and provide energy by minute to the brain by releasing inflammatory signals which are essential for normal memory signaling.   Unfortunately the virus can cause acute neurological symptoms and long-lasting impacts to the brain.   The virus requires alot of neuroinflammatory signaling.  Many neurological connections are destroyed and connections at gap junctions are destroyed which are needed to store memory.

Immune system and the brain

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.  The disruptive and destructive actions of neuroimmune cells and inflammatory signaling can permanently impair memory.

How does inflammation exert long-lasting effects on memory?

It will be many years before we know whether the COVID-19 infection causes an increased risk for cognitive decline or Alzheimer's disease.  These risks can be reduced by flu shots and vaccines.  Treatment can reduce the reduce the duration of the virus which will reduce the impact of the brain.

Does COVID-19 increase risk for cognitive decline?

cognition isn't just about thinking but also about brain function.  Many patients have experienced loss of smell, delirium and an increased risk of stroke.  Many experience long lasting effects of the brain.  Some topics to focus on would be as follows:
-  The immune system and the brain
-  How does inflammation exert long-lasting effects on memory?
-  Does COVID-19 increase risk for cognitive decline?

Ohio State University, Columbus

COVID-19 patients have reported mental fatigue and loss of concentration.  Severe cognitive impairment is reported by people with secondary illnesses.  Encephalopathy (damage to brain) is observed after extubation.  This could be because of sedation or mechanical ventilation.  Damage to the brain can occur from bacteria during ventilation. 
 



Cognitive impacts of COVID-19

Tronson, N. (2020, August 10). How COVID-19 might increase risk of memory loss and cognitive decline. Retrieved September 26, 2020, from https://medicalxpress.com/news/2020-08-covid-memory-loss-cognitive-decline.html

How COVID-19 might increase risk of memory loss and cognitive decline

It was found early on that population with respiratory problems is at greater risk but risk factors include pre-existing diagnoses such as dementia, subarachnoid hemorrhage and epilepsy.  Increased risk is found when the acute care uses sedation, ventilation and delirium. 


Who is likely to suffer from neurocognitive symptoms

Patients with MS are specifically vulnerable to the neuropsychiatric impacts of the COVID-19 pandemic. About 70% of multiple sclerosis patients suffer from cognitive dysfunction.  This affects information processing and impacts episodic memory. Depression and anxiety result in a lower quality of life, increased fatigue and disability scores, and a more aggressive MS course.  Studies show that depression impacts cognition and anxiety worsens the patient's verbal learning.

Neuropsychiatric and cognitive effects of COVID-19 on multiple sclerosis patients

COVID-19 is directly relevant to the cognitive health of the aging brain in a number of ways, including the effects of the disease, treatments, and current society. cause brain effects such as encephalopathy, similar to the 2002 Severe Acute Respiratory Syndrome, which showed seizures and brain tissue injury. COVID-19 causes respiratory failure, which is linked to increased risk of dementia due to a lack of oxygen to the brain.  Ventilators and sedation causes distress to cognition and causes delirium.  Long-term impaired memory and thinking are observed long after discharge as a result of post-traumatic stress.

A Tsunami of Dementia Could Be on the Way

Most researchers believe the neurological effect of the virus are an indirect result of either oxygen starvation to the brain (the “happy hypoxia” exhibited by many patients), or the byproduct of the body’s inflammatory response (the famed “cytokine storm”).  A pateints MRI brain scan showed signs of viral meningitis (inflammation of the brain), and a lumbar puncture detected Sars-CoV-2 in his cerebrospinal fluid.  Another patient had viral particals detected in the  endothelial cells lining the blood vessels of the brain itself. In fact, some scientists now suspect that the virus causes respiratory failure and death not through damage to the lungs but through damage to the brainstem.

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