Researchers found a link between COVID-19 & blood markers linked to faulty proteins in the brain. They found people who had previously had COVID-19 were more likely to have increased levels of biomarkers linked to faulty amyloid proteins—a hallmark for Alzheimer's disease. 1/
On average, the effects were comparable to 4 years of aging with the greatest effects seen in those hospitalized with severe COVID-19 or with underlying risk factors for dementia such as smoking or high blood pressure. 2/
The findings suggest that mild or moderate COVID may accelerate biological processes that contribute to buildup of disease-promoting amyloid in brain. This raises possibility that COVID-19 might contribute to an increase in later risks of developing Alzheimer's disease. 3/
These findings suggest COVID-19 may drive changes which contribute to neurodegenerative disease. This may be due to the inflammation triggered by the disease, although how this inflammation might impact the brain and changes to amyloid is not yet fully clear. 4/
However, the researchers can’t say that catching the SARS-CoV-2 virus directly causes these changes, or if it does, by how much a single episode of infection increases someone's risk. 5/
But these findings do suggest that COVID-19 may increase the risk of Alzheimer's in the future—as has been suggested in the past for other kinds of infections—especially among people with pre-existing risk factors. 6/
Amyloid is a common protein with a range of functions in the body. But the buildup of an abnormal form of the protein, called beta amyloid (Aβ), is a key component of many diseases. 7/
Aβ forms the characteristic clumps seen in the brains of patients with Alzheimer's disease, which are thought to cause damage to the neurons in the brain, leading to changes in cognition and behavior. 8/
In this study, the researchers found SARS-CoV-2 infection was associated w/ changes in several blood proteins previously linked to brain Aβ pathology. The magnitude of changes was similar to that associated w/ a well-known genetic risk factor for AD, a genetic variant: APOE4 9/
Greater changes found in older participants & those hospitalized with COVID-19-19 or had a history of hypertension. These correlated with poorer cognitive test scores & measures of overall health as well as changes in brain imaging patterns associated w/neurodegeneration 10/
More studies now are needed to prove any causal links. Ultimately, the more we know about factors that contribute to dementia risk—whether they are directly under our control, like lifestyle or diet, or modifiable by vaccines or early treatment for infectious diseases. 11/11
A small brain-imaging study found that people with #LongCOVID showed slower thinking and reaction times during a cognitive task.
➡️ Advanced MRI scans revealed changes in how important brain networks communicate with each other, especially those involved in attention, language, and decision-making. 1/
Researchers found altered connectivity in key brain networks:
• Salience network
• Language network
• Central executive network
• Sensorimotor and visual networks
➡️ These systems are essential for attention, decision-making, and task control. 2/
The most prominent deficits were seen in the salience network, which helps the brain detect and respond to important stimuli.
➡️ Connectivity problems in this network were more severe with longer illness duration. 3/
➡️ Compared with healthy controls,
✔ Long COVID patients had blunted morning cortisol peaks
✔ Higher evening cortisol
✔ Loss of normal circadian pattern
Blood cortisol alone failed to detect these changes. 2/
Key insight:
➡️ Salivary cortisol profiling may be a more sensitive marker of stress-system dysfunction in LongCOVID than standard blood tests.
➡️ HPA axis disruption could underlie:
• Fatigue
• Brain fog
• Sleep disturbance
• Dysautonomia. 3/
➡️ New review highlights that persistent cognitive symptoms in COVID survivors are strongly linked to pro-inflammatory cytokines and blood–brain barrier (BBB) dysfunction.
➡️ Key culprits include IL-6, TNF-α, IL-1β, IL-8, IL-13 and MCP-1 — many remain elevated months after infection.
🔥 COVID-19 is not just a respiratory disease.
➡️ Evidence suggests cognitive impairment can occur due to:
Post-COVID fatigue isn’t just subjective.
Using advanced MRI, researchers found real changes in brain blood flow and oxygen metabolism in people with Post-COVID-19 Syndrome (PCS) after mild infection.
➡️ Key finding:
PCS patients showed increased oxygen metabolism in the hippocampus (memory hub) but reduced metabolism in the anterior cingulate cortex (ACC) — despite no visible brain atrophy. 1/
Why this matters:
➡️ Higher hippocampal metabolism was linked to better cognitive performance, suggesting a compensatory response to maintain thinking and memory in PCS. 2/
In contrast, lower anterior cingulate cortex (ACC) metabolism correlated with: