A NEW study shows the onset of autism in COVID exposed babies at 28 months. Researchers found 23 of 211 children (11%), screened positive for autism spectrum disorder, compared with an expected prevalence of 1-2% at that age 1/
When researchers analyzed videos of children lying on their backs in what’s called General Movement Assessment, 14% of infants showed signs of developmental problems. The test evaluates early motor functions & is often used to assess the risk of neurodevelopmental disorders 2/
Later, the findings proved equally troubling. At 6-8 months old, 13 of 109 infants born to infected mothers — almost 12% — had failed to reach developmental milestones. In stark contrast, all infants in a control group born before the pandemic showed normal development. 3/
Around 11.6% of toddlers born to mothers with lab-confirmed SARS-CoV-2 infection during pregnancy showed cognitive, motor or language problems indicative of neurodevelopmental delays. By comparison, only two of 128 unexposed controls — 1.6% — showed such issues. 4/
When the eldest of the COVID-exposed babies reached 28 months, the study found another concerning pattern: 23 of 211 children — almost 11% — screened positive for autism spectrum disorder. 5/
The later findings, currently undergoing peer review ahead of publication, are a reminder that COVID’s long-term consequences, including higher risks for dementia and heart disease, continue to unravel almost five years after the pandemic began. 6/.
While the virus is generally known to cause more severe symptoms in adults than in children, emerging data suggest that babies exposed to COVID in utero face elevated risks for preterm birth, congenital heart abnormalities & rare conditions, such as situs inversus. 7/
Children born during the Covid era are now reaching the average age for autism diagnoses. Identifying developmental issues early can open the door to speech and behavioral therapies, which are proven to support a child’s development. 8/
Scientists say the full consequences of in utero exposure to the SARs-CoV-2 may take decades to uncover and understand. Even if a link is established, genetics are likely to play a crucial role. 9/
The researchers continue to analyze stored blood & other specimens from the babies in their study. “It’s a new pathogen. We don’t know how it behaves. Things might appear down the road that we were not expecting.” 10/10
Impact of COVID-19 on accelerating of immunosenescence & brain aging
The pandemic has highlighted a complex interplay between viral infection, immune aging & brain health, that can potentially accelerate neuroimmune aging & contribute to persistence of long COVID condition 1/
By inducing chronic inflammation, immunosenescence, and neuroinflammation, COVID-19 may exacerbate the processes of neuroimmune aging, leading to increased risks of cognitive decline, neurodegenerative diseases, and impaired immune function. 2/
Both aging & COVID-19 can induce neuroinflammation through the accumulation of senescent cells, persistent microglia and astrocytes’ activation, and increased pro-inflammatory cytokine production, such as IL-1β, IL-6, and TNF-α. 3/
Researchers have identified interleukin-23 receptor (IL-23R) as a significant biomarker of cellular senescence and aging. Experiments show that IL-23R levels in the bloodstream increase with age and can decrease, reflecting senescent cell clearing, with senolytic therapies. 1/
Cellular senescence occurs when cells stop dividing but do not trigger apoptosis mechanisms that would allow them to die naturally. 2/
Instead, they are stuck in a zombie-like state, where they still have the urge to feed and carry out metabolic activities, but with increasingly incoherent cell signaling and increased pro-inflammatory cytokine secretions. 3/
Coupling antigens from multiple subtypes of influenza can broaden antibody and T cell responses!
A novel vaccine platform that improved protection against diverse influenza subtypes when tested in animal models and human organoids. 1/
The seasonal influenza vaccine contains strains of viruses from distinct subtypes that are grown independently and then combined.
However, most individuals exhibit a more robust response to one of these strains and thus are vulnerable to infection by others. 2/
By studying a monozygotic twin cohort, the researchers found that although prior exposure was a factor, host genetics were a stronger driver of subtype bias to influenza viral strains. 3/
Clinical evidence suggests that SARS-CoV-2 directly disrupts vascular homeostasis, with perfusion abnormalities observed in various tissues. The pancreatic islet, a key endocrine mini-organ reliant on its microvasculature for optimal function, may be particularly vulnerable. 1/
Studies have proposed a link between SARS-CoV-2 infection and islet dysfunction, but the mechanisms remain unclear.
Here, researchers investigated how SARS-CoV-2 spike S1 protein affects human islet microvascular function. 2/
Using confocal microscopy and living pancreas slices from non-diabetic organ donors, they show that a SARS-CoV-2 spike S1 recombinant protein activates pericytes — key regulators of islet capillary diameter and beta cell function—and induces capillary constriction. 3/
Scientists have identified "immune pathways" during acute coronavirus infection that are associated with the development of #LongCOVID, and while some pathways are the same for men and women, others differ dramatically along a sharp divide between the sexes. 1/
A research team explored immune pathways in the development, persistence and resolution of longCOVID, say sex-based differences—and similarities—not only emerged in their research, the findings have helped shed new light on long COVID and suggest new paradigms for treatment. 2/
Some pathways, such as alterations in monocyte activation, were shared between the sexes.
Monocytes are immune cells that are part of the innate immune system—first responders—that fight infection and summon other components of the immune system to destroy invading viruses 3/
Common cough syrup ingredient offers hope for lung fibrosis!
A NEW study found that the best candidate is already available as a cough medicine around the world, #dextromethorphan. The study shows how dextromethorphan can impede collagen that forms scars inside cells. 1/
The study explored the potential of #Dextromethorphan in the treatment of lung fibrosis. Lung fibrosis occurs after accumulation of scar tissue in the lung (Lt: a mice lung w/ scarring tissue) which was reduced after treatment w/ Dextromethorphan (Rt). 2/
They performed an in vitro screen of FDA-approved drugs in primary human lung fibroblasts and found that dextromethorphan, a cough suppressant, could reduce fibrillar collagen deposition through inhibition of membrane trafficking of TGF-β–related proteins and collagens. 3/