The brain fog that can linger after a bout with COVID is not a new discovery. In fact, much research has linked this long-COVID symptom to the neuroinflammation that often accompanies an infection. However, scientists are now finding that this brain damage might be much more permanent, even leading to an increased risk of Alzheimer’s.
RELATED: Doctors Reveal the #1 Supplement to Reduce Dementia Risk.
How does COVID cause inflammation in the brain?
A study published last year in the journal Frontiers in Microbiology identified four ways that COVID infections in the lungs cause inflammation in the brain:
- Activation of an innate immune response: Inflammation is a well-known side effect when your body is fighting off a virus
- Disruption of the blood-brain barrier, which can allow toxins, pathogens, and inflammatory cells to enter the brain
- Damage to endothelial cells, those lining blood vessels that play a role in inflammation
- Disruption to the formation and functioning and nerve cells
As the American Brain Foundation explains, “brain cells are directly affected during a neuroinflammatory response, and a person can experience temporary changes in mental and emotional processes—thinking, concentration, behavior, mood, fatigue, motivation, and so on.”
They continue, “If inflammation becomes chronic, lasting or recurring for months or years, it can be a serious concern for patients. In chronic inflammation, the immune system may begin attacking healthy tissue.”
RELATED: COVID’s “Extreme Inflammatory Response” Can Hurt Your Heart, New Research Shows.
New research links COVID-related brain inflammation to Alzheimer’s disease.
Two new studies provide evidence that brain changes associated with COVID can increase the risk of developing Alzheimer’s disease.
First, a study published last month in the journal Frontiers in Aging Neuroscience found that the COVID virus and Chlamydia pneumonia, a bacterium that causes respiratory tract infections, “may predispose susceptible populations” to Alzheimer’s disease.
A press release published in News Medical explains that both infections increase cytokine levels in the brain.
“Cytokines are proteins that function as chemical messengers in your immune system,” notes Cleveland Clinic. “Too many cytokines can lead to excess inflammation and conditions like autoimmune diseases.”
The researchers found that both infections can invade the central nervous system through the blood-brain barrier, as well as through the olfactory system, which eventually connects to the areas of the brain responsible for memory and cognition.
“This pathway is particularly relevant given that loss of smell is an early symptom in both COVID-19 and Alzheimer’s disease,” states the press release.
RELATED: FDA Approves First-Ever Alzheimer’s Blood Test—Here’s Who Will Benefit.
Another study found that COVID can increase plaque buildup in the brain.
The other study, published in Science Advances, looked at the connection between COVID infections and amyloid plaques.
As News Medical explains, amyloid plaques are clumps of the protein beta-amyloid that form in the spaces between nerve cells in the brain: “These abnormally configured proteins are thought to play a central role in Alzheimer’s disease.”
To better understand this connection, researchers studied retinal tissue (that which lines the back of the eye) since they had previously determined that Alzheimer’s patients with an accumulation of amyloid beta in the brain also had an accumulation in the retina. They also determined that COVID can enter retinal cells.
In a review of the study, Medical Xpress explains, “Human retinal tissues collected from patients with COVID-19 but without any history of dementia also showed higher amyloid beta accumulation than that found in healthy individuals, to a degree similar to what the researchers found in retinal tissue from people with Alzheimer’s disease.”
Senior study author Brian Hafler, MD, Ph.D., associate professor of ophthalmology and visual science at Yale School of Medicine, told Medical Xpress that the finding “bolsters the amyloid beta antimicrobial hypothesis of Alzheimer’s disease, suggesting that amyloid beta could act as part of the brain’s innate immune response against viral infections.”
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