That’s according to a new study published this month in the journal Cell. Researchers from Weill Cornell Medicine, Memorial Sloan Kettering Cancer Center, and Columbia University used human stem cells to create cells from various organs, including the lung, heart, and pancreas. The virus was able to infect cells from all the aforementioned organs. But it did a particularly good job of infiltrating some types of neurons in the brain that produce dopamine—a neurotransmitter responsible for feelings of pleasure, motivation, memory, sleep, and movement. 

Once infected, such cells can lose their ability to grow and divide, researchers found. The cells also stop producing dopamine and instead send out signals that cause inflammation.

Because a loss of dopamine-producing neurons is associated with Parkinson’s disease—a slowly developing neurodegenerative condition that leads to tremors and, often, dementia—people who’ve been infected with COVID are at an increased risk of developing symptoms of the disorder at some point in their lives, the researchers wrote.

“We keep discovering new cell types that can be infected by the virus,” Dr. Shuibing Chen, professor of chemical biology in surgery at Weill Cornell Medicine and lead author on the study, tells Fortune. “We’re still trying to understand how it damages them. We need to keep the work ongoing, keep watching to see what happens.”

Regardless, the virus’s detrimental effect on dopamine neurons may explain neurologic symptoms in those with an active COVID infection, like headache, loss of smell, and a persistent unpleasant taste in the mouth, according to researchers.

It may also explain more immediate neurologic symptoms of long COVID, like brain fog, sleep issues, depression, and anxiety.

However grim the findings, the team’s study resulted in some positive news: ALS drug riluzole, diabetes drug metformin, and cancer drug imatinib appear to prevent the aforementioned type of neurons from becoming infected with COVID and, thus, losing their ability to function properly.

COVID’s unknown future consequences

Chen’s research adds to a growing body of evidence that COVID may affect human health long after the initial infection—in ways that aren’t associated with stereotypical long COVID, and that aren’t yet well understood.

While there is no one agreed upon definition of long COVID, it’s generally defined as the continuation of COVID symptoms or development of new symptoms within three months of initial infection. Symptoms last at least two months—and years, potentially—with no other explanation.

Long COVID is thought to typically present as a chronic-fatigue-syndrome-like condition similar to other post-viral syndromes that can develop after an infection—with herpes, Lyme disease, Ebola, the flu, and other pathogens. Hundreds of additional long COVID symptoms have been identified, however, everything from the COVID-like—such as dry cough and shortness of breath—to the bizarre—like hallucinations, ear numbness, and a sensation of “brain on fire.” 

Other post-COVID complications like long-term organ damage sustained during the virus’s acute phase should not be defined as long COVID and better fit under the larger umbrella category of PASC, or post-acute sequelae of COVID, some experts say.

Cellular damage, however, may not become apparent for months or years, as researchers are discovering. Aside from lung cells and some neurons, heart and colon cells can become infected with COVID, according to Chen, though the long-term implications are yet unknown. 

What’s more, COVID can alter cells—perhaps permanently. Chen’s team discovered as much in 2021, when they found that COVID infiltrates the pancreas’s insulin-producing beta cells, causing them to secrete less insulin and to start making glucagon—a hormone that, in contrast with insulin, raises blood glucose levels.

Other viruses may also increase Parkinson’s risk

The jury is still out as to whether COVID poses a heightened risk of future disease, or if other viruses have similar but underappreciated effects on a host’s health.

It’s not the only virus that may lead to an increased future risk of developing Parkison’s Disease-like symptoms, Chen points out. The Spanish flu pandemic of 1917–1918 is thought to have had a similar effect, and other viruses might as well.

While the COVID pandemic was unfortunate, “it gave us a pretty unique opportunity to focus on studying a disease in a very short period of time,” she says. Many, if not most, other pathogens haven’t received such dedicated research focus. Thus, others might have similar effects.

As for whether everyone who’s been infected with COVID—pretty much all of us, by now—is at greater risk of eventually developing Parkinson’s-like symptoms, it’s tough to say, according to Chen. Multiple factors can contribute to disease development, including genetics; age; gender; a history of head trauma; exposure to chemicals like pesticides and herbicides; Vietnam-era exposure to Agent Orange; a history of working with heavy metals, detergents, and solvents—and, it appears, prior COVID infection.

Chen cautions that her team’s study was completed with cells grown in a lab—not in the complex environment of the human body. The findings, however, were corroborated by autopsies of those who had been infected with COVID before death. 

Further study is needed, Chen says, to determine whether repeat COVID infection places people at a higher risk of Parkinson’s-like symptoms down the line, or increases the number of neurons damaged with each infection.

As for what the average person should do to protect their health, Chen advises decreasing the risk of COVID infection, whether that’s through masking or vaccination. The latter can limit the extent of infection—and perhaps the fallout from it—when a vaccinated person encounters the virus during daily life. 

If a person who has experienced COVID begins to develop Parkinson’s disease symptoms, she recommends they inform their doctor of both their symptoms and the fact that their prior COVID infection could be placing them at higher risk of the disorder.

“It won’t hurt to keep that in mind,” she says.

What are the early symptoms of Parkinson’s disease?

While most people with Parkinson’s disease are diagnosed after age 60, 5% to 10% of patients with the condition begin to experience symptoms before age 50—some as early as 20.

The first symptom may be a minor tremor in just one hand—or even your finger or chin—while you’re resting. Here are some other early tells, according to the Parkinson’s Foundation:

• Smaller handwriting than in the past
• Loss of smell
• Difficulty sleeping due to sudden involuntary movements
• Arms that don’t swing when you walk like they used to
• Stiffness in your arms, legs, or trunk
• Constipation
• A change in your voice that makes it very soft, breathy, or hoarse
• A new lack of facial expression
• Dizziness or fainting

As symptoms progress, people with Parkinson’s may find themselves experiencing more motor-related symptoms, like the following, according to the Cleveland Clinic:

• Slow movements (these aren’t due to muscle weakness, but to muscle control problems, experts say)
• Resting tremors
• “Lead-pipe rigidity,” described as “constant, unchanging stiffness when moving a body part”
• “Cogwheel stiffness,” which leads to a stop-and-go appearance of movements when lead-pipe rigidity is combined with tremors
• Stooping or hunching over
• Blinking less than usual
• Drooling
• Trouble swallowing

While there isn’t a cure for Parkinson’s, a variety of medications and treatments—like dopamine, medications that stimulate dopamine, medications like block dopamine metabolism, and deep-brain stimulation—can significantly improve symptoms. 

There are experimental treatments, too, like stem cell transplants, neuron-repair treatments, gene therapies, and gene-targeted treatments, meaning more hope should be on the horizon for Parkinson’s patients.