Infections can make our brain function much worse

Why did so many neurological symptoms appear after the 1918 flu pandemic? What is the explanation for the neuronal damage identified in patients with recurrent Covid-19? Neuroinflammation triggered by viral or bacterial infections is more common than we think. And it can damage the brain in the long term.

The inflammasome and the brain
When we age, our cells and tissues lose functionality and this loss of function is associated with well-known chronic diseases. One of the common denominators in this process is the accumulation of cellular waste that ends up causing the death of the cells and, as a consequence, the loss of capacity of the organ to which they belong.

The accumulation of damage can also lead to cellular senescence, which leads to the release of substances that cause inflammation.

Currently, many research groups are trying to discover anti-aging substances that reduce this senescence. In this search, they have detected that the activation of the inflammasome, a complex of proteins that promotes the release of inflammatory mediators such as the interleukins IL-1 and IL-18, is related to aging and practically all chronic diseases associated with it.

The activation of the inflammasome and the release of factors that produce inflammation are also linked to degenerative processes that affect the central nervous system and lead to cognitive deficiency and Alzheimer's.

For all these reasons, inflammation of the central nervous system, known as neuroinflammation, has become an important therapeutic target for the treatment of neurodegenerative diseases.

Causes of neuroinflammation
What causes the inflammasome to activate in some people and not in others? It depends on many factors. Some are internal, such as damage to mitochondria (cellular energy plants) or the accumulation of certain metabolites. But it is also activated by external factors, especially pathogens: viruses, bacteria and fungi. In other words, infections can cause the brain to swell and deteriorate.

The defenses that come to our aid can further aggravate the damage. Recent studies indicate that invasion of nervous tissue by activated cells of the immune system may also contribute to inflammation and cognitive decline. In addition, when activated T lymphocytes flock to the brain, Tau protein accumulates within neurons, another of the hallmarks of Alzheimer's disease.

In addition, there are certain genetic factors associated with Alzheimer's, for example variations in the cholesterol-transporting protein APOE4, which have recently been linked to a pro-inflammatory profile in endothelial cells. That would explain part of the neuroinflammation and the increase in beta-amyloid protein deposits around neurons.

Infections, vascular damage and neuroinflammation
A thin layer made up of very flat epithelial cells separates the blood flow from the inside of the organs. These cells are called vascular endothelium and fulfill a very important function: regulating the passage of substances and cells from the blood to the organs.

In the central nervous system, this wall of cells, known as the blood-brain barrier, has peculiar characteristics. To begin with, it is made up of endothelial cells, smooth muscle cells, cells called pericytes, connective tissue and astrocytes. All of them establish close connections between themselves, controlling the flow of substances and cells to and from the central nervous system.

The loss of the properties of this barrier has been associated with different neuronal diseases, including stroke, multiple sclerosis, traumatic brain injury and its repercussions, and neurodegenerative diseases.

It is clear that any agent that causes damage to the vascular endothelium and, especially, that which forms the blood-brain barrier can trigger neuroinflammation and neurodegenerative processes. On the other hand, it is not unusual for viral and bacterial infections to cause damage to blood vessels, including those of the brain, leading to accelerated atherosclerosis, inflammation of the vessels (vasculitis) or coagulopathies. This can lead to strokes or strokes in the short term.

But these same infections can also cause inflammatory processes that end up activating immune system cells that, in turn, invade nervous tissue through a damaged blood-brain barrier, generating chronic neuroinflammation and long-term damage.

Another factor to take into account is that endothelial damage increases the more years we accumulate behind us and, in addition, it accelerates in metabolic diseases such as metabolic syndrome. That would explain why covid-19 and other infectious diseases have been shown to be more serious in obese and/or elderly people.

Can vaccination campaigns prevent neurodegeneration?
Based on what we have just explained, we can conclude that preventing endothelial damage after infections is essential to reduce neuroinflammation and, as a consequence, reduce the neuronal damage that causes Alzheimer's and other neurodegenerative diseases.

In fact, some natural compounds such as polyphenols, vitamin C and even Coenzyme Q10 have been proposed as substances that maintain the stability of the vascular endothelium and protect the brain.

But if we also take into account that vaccines prevent serious symptoms due to infections and prevent microorganisms from reaching the bloodstream, we can hypothesize that the vaccines that began to be generally introduced in the 60s or 70s may have reduced the damage. vascular diseases that lead to neurodegeneration.

Currently, most elderly people were not part of these vaccination campaigns in their childhood. So we will have to wait another 20 or 30 years to see if diseases such as Alzheimer's or Parkinson's decrease their prevalence in the vaccinated population.

If confirmed, we could conclude that preventing certain infections and maintaining the health of the vascular endothelium is essential to reduce the incidence of degenerative diseases even in the very long term.

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Source: The Conversation. Authorship:

Guillermo López Lluch
Professor in the area of ​​Cellular Biology. Associate researcher at the Andalusian Center for Developmental Biology. Researcher in metabolism, aging and immune and antioxidant systems, Pablo de Olavide University