Long COVID Linked to Brain Changes Associated with Alzheimer’s Disease, New Study Finds
A concerning new study reveals a potential link between long COVID and an increased risk of Alzheimer’s disease, with researchers identifying structural changes in the brain and elevated biomarkers associated with neurodegeneration in individuals experiencing prolonged symptoms following a SARS-CoV-2 infection.
Long COVID, affecting an estimated 780 million people globally, is characterized by a wide range of persistent symptoms, including fatigue, “brain fog,” and cognitive impairment. Now, research led by NYU Langone Health suggests these neurological manifestations may be tied to alterations in a critical brain structure called the choroid plexus (ChP).
The study, published in Alzheimer’s & Dementia, discovered that patients reporting long COVID had a 10% larger ChP compared to those who had fully recovered from their initial COVID-19 infection. This enlargement was coupled with reduced blood flow through the ChP’s blood vessels. “Our work suggests that long-term immune reactions caused in some cases after an initial COVID infection may come with swelling that damages a critical brain barrier in the choroid plexus,” explained a senior researcher at the NYU Grossman School of Medicine.
The ChP plays a vital role in brain health, serving as the primary site for cerebrospinal fluid (CSF) production, regulating immune responses, and maintaining the blood-CSF barrier. Damage to this structure can disrupt these crucial functions. Researchers found that the increased ChP size correlated with elevated levels of specific proteins in the blood – glial fibrillary acidic protein (GFAP) and pTau217 – both of which are known indicators of brain injury and Alzheimer’s disease progression.
“GFAP, an astrocytic biomarker, elevated during neuronal injury, glial activation, and scarring, is recently considered as potential biomarker of AD,” the research team noted. Plasma p-tTau217 is a highly sensitive biomarker for identifying AD, reflecting both amyloid and tau burden. Furthermore, patients with larger ChPs exhibited a modest, but statistically significant, decline in cognitive performance, scoring an average of two percent lower on the Mini-Mental State Exam (MMSE), a standard test assessing memory and attention.
The team recruited 179 participants for the study, including 86 individuals with neurological symptoms of long COVID, 67 who had recovered from COVID-19, and 26 who had never been infected. Participants underwent advanced brain MRI scans, blood tests, and cognitive assessments to allow for a comprehensive comparison. The researchers analyzed structural and perfusion alterations in the ChP, exploring their relationship to neurological symptoms and biomarkers.
The underlying mechanism driving these changes remains under investigation, but the researchers hypothesize that inflammation-driven vascular remodeling within the ChP is a key factor. This process involves the thickening of blood vessel walls due to prolonged immune activation and the buildup of scar-like tissue, hindering blood flow. Impaired blood perfusion in the ChP could then compromise CSF production, lead to waste accumulation, and weaken the blood-CSF barrier.
“In conclusion, we identified ChP alterations in long COVID, characterized by enlarged volume and reduced blood flow. These alterations were associated with sleep disturbances, cognitive impairment, and plasma biomarkers of AD, suggesting a potential link to future dementia risk,” the scientists reported.
Acknowledging the limitations of their study, the investigators emphasized the need for further research to confirm these findings and clarify the long-term implications. “Our next step is to follow these patients over time to see if the brain changes we identified can predict who will develop long-term cognitive issues,” said a co-senior study author. “A larger, long-term study will be needed to clarify whether these CP alterations are a cause or a consequence of the neurological symptoms, which promises to better focus treatment design efforts.”
This research underscores the complex and potentially far-reaching neurological consequences of COVID-19, raising concerns about a possible surge in Alzheimer’s disease cases in the years to come.
