In a study that reshapes what we know about COVID19, scientists have discovered that coagulation protein fibrin causes unusual clotting & inflammation that have become hallmarks of the disease, while also suppressing the body's ability to clear virus.
Importantly, the team also identified a new antibody therapy to combat all of these deleterious effects. The study by overturns the prevailing theory that blood clotting is merely a consequence of inflammation in COVID-19.
Through experiments in the lab and with mice, the researchers show that blood clotting is instead a primary effect, driving other problems—including toxic inflammation, impaired viral clearance, and neurological symptoms prevalent in those with COVID-19 and long COVID.
In this study, scientists found that fibrin becomes even more toxic in COVID-19 as it binds to both the virus and immune cells, creating unusual clots that lead to inflammation, fibrosis, and loss of neurons.
Knowing that fibrin is instigator of inflammation & neurological symptoms, we can build a new path forward for treating the disease at the root. In their experiments, neutralizing blood toxicity with fibrin antibody therapy can protect the brain and body after COVID infection.
As fibrinogen plasma levels in acute COVID-19 are a predictive biomarker for cognitive impairment in longCOVID, it could be used to stratify patients as candidates for entry into phase 2 trials.
Fibrin immunotherapy can be tested for its potential to reduce adverse health outcomes due to long COVID as part of a multipronged approach with prevention and vaccination measures.
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/
➡️ New research shows that paternal SARS-CoV-2 infection before conception can alter sperm RNA — leading to anxiety-like behavior & brain gene changes in offspring.
A biological “memory” of infection may pass across generations. 1/
Beyond infection: inheritance
➡️ Male mice infected with SARS-CoV-2 fathered pups with altered hippocampal transcriptomes & higher anxiety.
Injecting sperm RNA from infected males reproduced the same effects — clear evidence of RNA-based inheritance. 2/
COVID’s unseen legacy
➡️ Study suggests COVID infection in fathers may have transgenerational effects via changes in sperm small RNAs.
Adds a new layer to how pandemics shape health — not just for one generation, but possibly the next. 3/
A new study provides new evidence to help us redefine steroid use in TB care
➡️ Given the renewed interest in the steroid dexamethasone, as a host-directed treatment during the COVID-19 pandemic, the Trinity College Dublin team provides evidence that treating patients with steroids may enhance the function of their macrophages to kill the mycobacteria, while diminishing pathways of inflammatory damage. 1/
The researchers goal was to determine whether dexamethasone impacts the macrophage's ability to fight TB. Although glucocorticoids can reactivate TB, they are paradoxically the only adjunctive host-directed therapies that are recommended by WHO for TB.
Steroids are given to patients alongside antimicrobials in certain circumstances; however, scientists don't fully understand the effect of these drugs on the immune system, especially innate immune cells such as macrophages. 2/
The researchers studied macrophages derived from the blood of healthy volunteers or isolated from lung fluid donated by patients undergoing routine bronchoscopies.
➡️ By treating and infecting these macrophages in the lab with Mtb, the scientists could examine and understand how dexamethasone affects the immune response that protects the lungs during infection. 3/