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
#LongCOVID: Not only a living nightmare, but a most neglected entity!
LongCOVID is costing countries billions of dollars a year in lost productivity & increased health and social welfare spending. 1/
One analysis of 8 countries by Economist media group suggested longCOVID could have cut their GDP by between 0.5% & 2.3% last year.
They have described it as "a mass disabling event", but a dearth of data makes it hard to gauge the economic impact & estimates vary wildly. 2/
The absence of a universal longCOVID definition worsens the issue. Patients have reported >200 symptoms involving the whole body. They include cognitive impairment, extreme fatigue, dyspnea, cardiac difficulties & joint discomfort.The cause is unknown and there's no cure. 3/
Is it possible to halt childhood brain tumor before it forms?
Researchers have found a strategy to prevent medulloblastoma, the most prevalent juvenile malignant brain cancer, from growing. They find a protein that wakes up'sleeping' stem cells and drives tumor growth. 1/
Brain cancer presents a unique set of challenges for researchers—by the time a person experiences symptoms, the tumors are often so complex that the fundamental mechanisms driving the tumor growth are no longer easy to identify. 2/
A research team working to combat this challenge for sonic hedgehog (SHH) medulloblastoma.
The researchers identify that a protein #OLIG2 is responsible for the waking up of 'sleeping' stem cells and driving SHH medulloblastoma tumor formation and regrowth. 3/
Why SARS-CoV-2 bounces back after #Paxlovid treatment
A NEW study found that the antiviral treatment, especially when given early in the course of the infection, can leave behind target cells that can still be infected with the virus. 1/
In addition, the treatment may not completely clear the virus, leaving behind infectious particles that invade the target cells. 2/
If at the end of 5 days of treatment, there's still virus and target cells around, then the infection can basically restart. Though the antiviral stops existing viruses from replicating, it doesn't remove the viral particles or the infected cells. 3/
Oxygen is essential for human life, yet a growing body of preclinical research is demonstrating that chronic continuous hypoxia (low levels of oxygen in your body tissues) can be beneficial in models of mitochondrial disease, autoimmunity, ischemia, and aging. 1/
This research is revealing exciting new and unexpected facets of oxygen biology, but translating these findings to patients poses major challenges, because hypoxia can be dangerous. 2/
Overcoming these barriers will require integrating insights from basic science, high-altitude physiology, clinical medicine, and sports technology. 3/
SARS-CoV-2 can be found in the pancreas following infection. In a NEW study, researchers investigated whether the pancreas is damaged by the infection & whether there are changes of the pancreatic enzymes that the pancreas produces & circulates around the rest of the body. 1/
A particular protein called the placenta-associated protein 8 (PLAC8) expression was found in people who died following SARS-CoV-2 infection. Researchers show this protein is required for SARS-CoV-2 pancreatic infection and viral replication. 2/
Their findings indicate that the human pancreas as a SARS-CoV-2 target with plausible signs of injury and demonstrate that the host factor PLAC8 is required for SARS-CoV-2 pancreatic infection 3/
👇SARS-CoV-2 infects pancreatic cell lines in a PLAC8-dependent manner.
Many treatments for autoimmune disorders cause systemic immunosuppression, leading to severe & chronic toxicities.
If immunity could be suppressed locally, only in targeted tissues, this could provide overcome these systemic toxicities to treat such diverse diseases 1/
🔥 Now, researchers have found a way to circumvent toxicities of systemic immunosuppression. They have engineered synthetic suppressor T cells that execute locally targeted immunoprotective programs. 2/
In theory, cell-based treatments could be set up to protect specific tissues from immune attack without immunosuppression. To make tailored suppressor cells, one could direct endogenous cells, like regulatory T cells or myeloid suppressor cells, to find disease sites.