The aftermath of the novel coronavirus is likely to persist for a long time.
It is estimated that over 20 million Americans are grappling with a debilitating condition that follows infection, often referred to as long COVID. Symptoms can include intense fatigue, breathing difficulties, chest pain, heart palpitations, dizziness, and muscle aches.
Recently, new research from NYU Langone Health sheds light on why some individuals may suffer from persistent “brain fog” or memory issues even after recovering from the virus.
Researchers are suggesting that prolonged COVID-19 infection might lead to brain changes akin to those observed in Alzheimer’s disease.
Dr. Yulin Ge, a professor of Radiology at NYU Grossman School of Medicine, stated, “Our findings indicate that the long-lasting immune response triggered by the coronavirus may result in swelling that compromises the crucial brain barrier, known as the choroid plexus (CP).”
He added, “There’s physical, molecular, and clinical evidence suggesting that an enlarged CP could serve as an early warning for cognitive decline similar to that seen in Alzheimer’s disease.”
The CP is a crucial network located within the brain’s ventricles, responsible for producing cerebrospinal fluid (CSF) and forming a barrier between blood and CSF.
This fluid plays a vital role in cushioning the brain and spinal cord, eliminating waste, and delivering essential nutrients.
The study monitored 86 patients who experienced ongoing neurological symptoms after COVID-19, compared to 67 who fully recovered from the virus without lasting symptoms and 26 healthy individuals who had never been infected.
Results indicated that those with long-term COVID-19 symptoms exhibited a 10% increase in CP size compared to the recoverees.
Interestingly, a larger CP is not necessarily better. It’s considered a significant indicator of ongoing neuroinflammation and degeneration.
This increase has been linked to Alzheimer’s disease biomarkers, including elevated phosphorylated tau (pTau217) and glial fibrillary acidic protein (GFAP), which could rise after incidents like traumatic brain injuries or strokes.
Patients with a larger CP scored about 2% lower on a cognitive test out of 30 points.
The expansion of the CP can restrict blood flow, hindering CSF production and the brain’s ability to eliminate waste effectively.
Research indicates that the new coronavirus may inflict damage on the CP. Ge mentioned that alterations in CP are also observed in infections like viral meningitis and HIV.
His team has proposed that long-lasting coronavirus infections might lead to chronic inflammation, causing the blood vessels in the CP to thicken.
“It’s still uncertain if these changes can be reversed. We’re currently analyzing data to explore this question,” Ge remarked.
This study was published in the journal Alzheimer’s & Dementia.
Dr. Thomas Wisniewski, a senior author from NYU Grossman School of Medicine, stated, “Our next step will involve monitoring these patients over time to determine whether the brain changes we’ve identified can anticipate the onset of long-term cognitive issues.”
“Further large-scale studies will be necessary to clarify whether these alterations in CP are a cause or a result of neurological symptoms, which could lead to more targeted treatment strategies.”
