COVID-19 Can Increase Future Risk of Neurodegenerative Diseases

Image of the brain Andrus Ciprian/Shutterstock

In research led by the University of Queensland (UQ), COVID-19 was shown to activate the same inflammatory response in the brain as Parkinson’s disease and create a future potential risk for neurodegenerative conditions.

Prof. Trent Woodruff, who led the research team of over 33 scientists from across UQ and around the world, said in a news release that when the team infected brain immune cells with SARS-CoV-2, which is the virus responsible for COVID-19, they discovered that the cells became aggravated.

“We found the cells effectively became ‘angry,’ activating the same pathway that Parkinson’s and Alzheimer’s proteins can activate in disease, the inflammasomes,” Woodruff said.

The activation of the inflammasome pathway, research team member Eduardo Albornoz Balmaceda PhD, explained, ignites a fire in the brain, beginning the sustained and persistent process of neuron destruction.

“It’s kind of a silent killer because you don’t see any outward symptoms for many years,” Albornoz Balmaceda said, noting that it may “explain why some people who’ve had COVID-19 are more vulnerable to developing neurological symptoms similar to Parkinson’s disease.”

Co-leading the research was Alberto Amarilla Ortiz PhD and Assoc. Prof. Daniel Watterson.

A COVID-19 infected mouse brain showing 'angry' microglia in green and SARS-CoV-2 in red. Image Supplied by Eduardo Albornoz Balmaceda/UQ

What COVID-19 Does to the Brain

In an email to The Epoch Times, Albornoz Balmaceda and Woodruff said that the team studied how the virus affected the immune cells of the brain, which are called “microglia,” and they are the principal cells involved in the progression of brain diseases such as Parkinson’s disease (PD) and Alzheimer’s.

“Microglial are everywhere in the brain but don’t attack neurons directly themselves,” Albornoz Balmaceda and Woodruff said.

“They are immune cells whose main job is to defend us from pathogens and in some instances from “bad proteins” like alpha-synuclein.”

Alpha-synuclein is a protein that is present in multiple neurodegenerative disorders such as Parkinson’s disease and dementia-related disorders. Its abundant in the brain and is predominantly located at the tip of neurons in structures called presynaptic terminals; these terminals release chemical messengers called neurotransmitters from receptacles named synaptic vesicles. 

The function of alpha-synuclein is not well known. However, studies have suggested multiple possibilities, such as responsibility for maintaining a sufficient number of synaptic vesicles or assisting in regulating dopamine release. 

“As a consequence of this activation, proinflammatory molecules are released that can kill the pathogens,” said Albornoz Balmaceda and Woodruff.

“The problem arises when these cells are activated in a chronic and uncontrolled manner.

“This inflammatory environment can then start indirectly killing neurons. The type of neurons and brain area that are going to be affected will characterise the disease; for example, in the case of PD are dopaminergic neurons,” they said.

Millions of people are still nursing themselves in the aftermath as they recover from spike protein injuries. Illustration of the spike protein of SARS-CoV-2. Juan Gaertner/Shutterstock

Effect of COVID-19 on a Brain with Alpha-Synuclein

Although the team discovered that the spike protein of the COVID-19 virus was sufficient to initiate the neuron destruction process, the presence of proteins linked with Parkinson’s did have an effect.

“From our laboratory research, we showed that SARS-CoV-2 can activate the same inflammatory pathway that is triggered in PD,” said Albornoz Balmaceda and Woodruff.

“Interestingly, when we induced SARS-CoV-2 infection in presence of alpha-synuclein (a protein present in PD) the pathway activation was exacerbated.

“We don’t have clinical evidence to compare the degree of inflammation between COVID-19 infection and PD. However, PD is a long-term chronic disease, unlike acute COVID-19 infection.”

Therefore, Woodruff said that for people who already have a predisposition for Parkinson’s disease, experiencing a COVID-19 infection could be like pouring more fuel on a fire.

“The same would apply for a predisposition for Alzheimer’s and other dementias that have been linked to inflammasomes.”

Woodruff said that despite the alarming nature of uncovering similarities between the brain's response to COVID-19 and its response to dementia diseases, this discovery also meant that a possible treatment already exists. A nurse holds the hands of a patient in a 2009 file photo. Sebastien Bozon/AFP/Getty Images

Treating the Condition

Woodruff said that despite the alarming nature of uncovering similarities between the brain’s response to COVID-19 and its response to dementia diseases, this discovery also meant that a possible treatment already exists.

The research team discovered that an existing class of inhibitory drugs, which were developed at UQ, are able to treat the neurodegeneration that is brought on by COVID-19. The drugs are currently undergoing clinical trials as an experimental treatment for Parkinson’s.

“We found it successfully blocked the inflammatory pathway activated by COVID-19, essentially putting out the fire,” Albornoz Balmaceda said.

“The drug reduced inflammation in both COVID-19-infected mice and the microglia cells from humans, suggesting a possible treatment approach to prevent neurodegeneration in the future.”

“Further research is needed, but this is potentially a new approach to treating a virus that could otherwise have untold long-term health ramifications.”

When asked if people experiencing brain fog following COVID should visit a medical practitioner and whether an early diagnosis is important for this condition, Albornoz Balmaceda and Woodruff noted while they were not doctors, it was wise to consult a medical professional.

“It is always good to enquire with medical professionals when a medical issue arises that is of concern to the individual,” they said.

The study, “SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike protein,” was published in Molecular Psychiatry, on Nov. 1.