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
Can past COVID-19 weaken the body’s ability to fight tuberculosis?
➡️ A new study comparing immune responses to SARS-CoV-2 and Mycobacterium tuberculosis (MTB) suggests COVID-19 may dampen both antiviral and anti-TB immunity — even months later. 1/
Researchers tested immune cells from healthy individuals and COVID-19 survivors, both with and without latent TB infection (LTBI).
➡️ They stimulated the cells with SARS-CoV-2 Spike and MTB antigens and measured cytokine responses. 2/
Key finding:
➡️ People who recovered from COVID-19 showed significantly reduced inflammatory cytokines — IFN-γ, IL-2, IL-6, TNF-α — in response to both SARS-CoV-2 and MTB antigens.
➡️ Suggests prolonged immune downregulation after COVID-19. 3/
A new study comparing immune profiles months after COVID-19 vs influenza shows that SARS-CoV-2 leaves behind distinct and longer-lasting immune abnormalities — very different from what is seen after flu. 1/
Post-COVID patients showed increased CXCR3 and CCR6 expression across multiple lymphocyte populations.
➡️ Punjabi This means their immune system is still sending signals for cells to migrate into tissues (especially the lungs) months after infection.
In contrast, post-flu patients mainly showed a decrease in CCR4 on naïve T cells, monocytes, and dendritic cells — a very different and less persistent pattern.
➡️ Flu does not drive the same long-term immune activation. 3/
A new study provides some of the strongest evidence yet that mitochondrial dysfunction can directly cause #Parkinson’s disease, rather than being a consequence of neuron loss.
➡️ Researchers used a unique mouse model carrying a mutation in CHCHD2, a mitochondrial protein linked to a rare inherited form of Parkinson’s that closely mimics the common, late-onset form. 1/
Key Findings
➡️ Mutant CHCHD2 accumulates in mitochondria, making them swollen and structurally abnormal.
➡️ Cells shift away from normal energy production and develop oxidative stress due to buildup of reactive oxygen species (ROS).
➡️ Alpha-synuclein aggregation occurs after ROS rises, suggesting oxidative stress triggers Lewy body formation.
➡️ Human brain tissue from people with sporadic Parkinson’s showed CHCHD2 accumulation inside early alpha-synuclein aggregates, confirming relevance beyond the rare genetic form. 2/
Implications
➡️ This work maps a step-by-step causal chain:
CHCHD2 mutation → mitochondrial failure → metabolic shift → ROS buildup → alpha-synuclein aggregation → Parkinson’s pathology
➡️ It supports the idea that mitochondrial defects may underlie many forms of Parkinson’s, not just the inherited type.
➡️ Targeting oxidative stress, mitochondrial health, and energy pathways could offer new therapeutic strategies. 3/
New research in Cell Reports Medicine helps explain why women are more likely to develop #LongCOVID — and often experience more severe, persistent symptoms like fatigue, brain fog, and pain.
The key? Differences in the immune system, gut, and hormones. 1/
Researchers studied 78 people with LongCOVID (mostly mild initial cases) and compared them to 62 who recovered fully.
➡️ One year later, women with Long COVID showed clear biological differences — especially signs of gut inflammation and “leakiness.” 2/
The study also found anemia and hormone imbalances.
Women with LongCOVID had lower testosterone — a hormone that normally helps control inflammation.
➡️ Lower testosterone was linked to more fatigue, pain, brain fog, and depression. 3/
➡️ Long COVID isn’t one disease — it’s a complex web of immune, vascular, and metabolic dysfunctions.
From fatigue & brain fog to heart & lung complications, it stems from viral persistence, autoimmunity, and mitochondrial damage. 1/
Proposed mechanisms:
1️⃣ Persistent viral reservoirs or antigen remnants
2️⃣ Reactivation of latent viruses (e.g., EBV)
3️⃣ Immune dysregulation & autoimmunity
4️⃣ Endothelial injury and microclots
5️⃣ Gut microbiome imbalance
6️⃣ Mitochondrial dysfunction and energy metabolism impairment. 2/
Current management:
- largely symptomatic—rehabilitation, pacing, and supportive therapies.
-Emerging treatments: under study — antiviral drugs, immune-modulating agents, microbiome restoration, and mitochondria-targeted therapies.
-Vaccination: reduces risk and severity of LongCOVID. 3/