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 pioneering study has demonstrated for the first time that myocardial infarction may be an infectious disease. This discovery challenges the conventional understanding of the pathogenesis of myocardial infarction and opens new avenues for treatment, diagnostics, and even vaccine development. 1/
According to the study, an infection may trigger myocardial infarction. Using a range of advanced methodologies, the research found that, in coronary artery disease, atherosclerotic plaques containing cholesterol may harbor a gelatinous, asymptomatic biofilm formed by bacteria over years or even decades. Dormant bacteria within the biofilm remain shielded from both the patient's immune system and antibiotics because they cannot penetrate the biofilm matrix. 2/
Of the bacteria detected, oral viridans group streptococcal DNA was the most common, being found in 42.1% of coronary plaques and 42.9% of endarterectomies. Immunopositivity for viridans streptococci correlated with severe atherosclerosis (P<0.0001) in both series and death from coronary heart disease (P=0.021) or myocardial infarction (P=0.042). 3/
According to a new study, SARS-CoV-2 virus hijacks the machinery of testicular cells that produce the hormone testosterone in order to replicate.
It also appropriates the metabolic pathways of these cells and cholesterol, a precursor of testosterone, thereby altering lipid metabolism for its formation. 1/
The study revealed the presence of SARS-CoV-2 particles in lipid inclusions and organelles responsible for testosterone production in Leydig cells for the first time.
In addition, the researchers described the mechanism by which the virus interferes with the functioning of these testicular cells.
The discovery helps explain why male patients with severe COVID-19 have lower levels of testosterone, and possibly cholesterol. 2/
After infecting the Leydig cells in the testicles, the virus uses lipid metabolism pathways and the cell structure to replicate, which impairs testosterone production.
This happens because these cells, responsible for producing testosterone, express high concentrations of the ACE2 receptor, facilitating the entry of the virus, 3/
A COVID infection, particularly in women, may lead to blood vessels aging around five years!
➡️ Blood vessels gradually become stiffer with age, but the new study suggests that COVID could accelerate this process. Researchers say this is important since people with stiffer blood vessels face a higher risk of cardiovascular disease, including stroke and heart attack. 1/
Since the pandemic, we have learned that many people who have had COVID are left with symptoms that can last for months or even years. However, we are still learning what's happening in the body to create these symptoms. 2/
It is known that COVID can directly affect blood vessels. This may result in what we call early vascular aging, meaning that your blood vessels are older than your chronological age and you are more susceptible to heart disease.
If that is happening, we need to identify who is at risk at an early stage to prevent heart attacks and strokes. 3/
🔥 A fascinating tale that reinforces the power of research driven by curiosity without preconceived notions.
➡️ For a few dozen people in the world, the downside of living with a rare immune condition comes with a surprising superpower—the ability to fight off all viruses.
➡️ An immunologist from Columbia discovered the individuals' antiviral powers about 15 years ago, soon after he identified the genetic mutation that causes the condition. 1/
At first, the condition only seemed to increase vulnerability to some bacterial infections. But as more patients were identified, its unexpected antiviral benefits became apparent.
The researcher soon learned that everyone with the mutation, which causes a deficiency in an immune regulator called IFN-I–stimulated gene 15 (ISG15), has mild but persistent systemic inflammation. 2/
The type I interferon (IFN-I) response is a conserved cascade of signaling and gene expression that, among other functions, confers protection of cells from viral infection.
After resolution of infection, the response is tamped down by regulators such as IFN-I–stimulated gene 15 (ISG15).
Cells from individuals lacking ISG15 are able to control viral infections in vitro as a consequence of maintaining a low-grade IFN-I response. 3/
In a small trial, researchers have found that a drug designed to treat celiac disease supported a more rapid return to normal activities for patients following COVID. The researchers found the oral drug #larazotide—an experimental drug originally designed to treat celiac disease—was both safe and effective in treating children with MIS-C. 1/
Current MIS-C treatments are limited. Some patients receive general anti-inflammatory drugs, but many experience a rebound of symptoms after completing a course. Such drugs are not designed to target the sticky SARS-CoV-2 viral particles that may persist in the gut. 2/
Enter larazotide, an orally administered drug that does target the gut. Larazotide strengthens intestinal barriers to limit the number of materials—like SARS-CoV-2 viral particles—that exit the intestines and enter circulation. 3/
Researchers have discovered that gut bacteria produce a molecule that not only induces but also causes atherosclerosis, the accumulation of fat and cholesterol in the arteries that can lead to heart attacks and strokes.
This unexpected link between microbes and cardiovascular disease — the leading cause of death in humanity — is a paradigm shift. 1/
The new results show that some gut bacteria, in certain states, produce imidazole propionate, a simple molecule with six carbon atoms, eight hydrogen atoms, two nitrogen atoms, and two oxygen atoms (C₆H₈N₂O₂). This compound enters the blood, interacts with immature white blood cells, and triggers an inflammatory reaction in the arteries, which promotes the buildup of fatty plaques. Imidazole propionate induces atherosclerosis on its own. There’s a causal relationship. 2/
Furthermore, scientists observed elevated levels of imidazole propionate in one out of every five volunteers with active atherosclerosis, the type in which fatty plaques are more likely to rupture and form the blood clots that cause heart attacks and strokes. The new results demonstrate that atherosclerosis is not only a disease caused by fat, but that it also has an inflammatory and autoimmune component. 3/