A NEW nasal spray that trap & neutralize not only SARS-CoV-2, Influenza, RSV, Adeno & many other viruses & bacteria that are inhaled into the nose, immobilizing them until they die. The substance is >99.9% effective & contains no drugs 1/
The FDA approved substance in the spray is known as the Pathogen Capture and Neutralizing Spray (PCANS), & contains no drugs of any kind.
Instead, the spray forms a gel that lines the inside of the nose. 2/
While this gel doesn't affect the user's breathing, it does trap any viruses or bacteria that are subsequently inhaled into the nose, immobilizing them until they die. 3/
In lab tests, the spray protected mice from a mouse-adapted form of the H1N1 influenza virus, even when that virus was administered at 25 times the lethal dose. 4/
What's more, virus levels in the animals' lungs were reduced by over 99.99% as compared to an untreated control group of mice. The spray was retained in the rodents' noses for up to eight hours, and was effective at blocking infection for at least four hours. 5/
Although PCANS has yet to be tested on humans, it has been used in a 3D-printed model of a human nose, where it captured twice as many microbe-containing droplets as mucus alone. 6/
It blocked and neutralized almost 100% of all viruses and bacteria we tested, including influenza, SARS-CoV-2, RSV, adenovirus, K Pneumonia and more. 7/
And if you suffer from allergies, take note – the researchers believe the spray could one day also be used on a daily basis to trap and neutralize allergens. 8/8
#LongCOVID (LC) shares striking symptom overlap with hypermobility spectrum disorders (HSD/hEDS): fatigue, brain fog, dysautonomia, pain—especially in women.
➡️ A new case series explores whether some “intractable” LC may reflect undiagnosed hypermobility disorders.
➡️ Five women with persistent LC symptoms were evaluated at an hEDS/HSD clinic.
All met Beighton score criteria for hypermobility.
➡️ 4 diagnosed with hEDS, 1 with HSD
➡️ 3 had dysautonomia
None had prior hypermobility diagnoses. 1/
All patients carried MTHFR polymorphisms (C677T or A1298C)—recently linked to hEDS/HSD.
➡️ Several also showed features of mast cell activation, suggesting immune dysregulation may unmask latent connective tissue disorders after SARS-CoV-2 infection.
➡️ Targeted management (physical therapy, methylfolate/B12, mast cell stabilization, pain interventions) led to clinical improvement in all cases.
🔑 Takeaway: Consider hEDS/HSD in women with refractory Long COVID, especially with multisystem pain and dysautonomia. 2/
This case series suggests that some patients with severe, persistent #LongCOVID—especially women—may have previously undiagnosed hypermobility disorders (hEDS/HSD).
➡️ Five women with refractory LongCOVID symptoms were found to meet criteria for hypermobility, often with dysautonomia, mast cell–related features, and MTHFR polymorphisms.
➡️ Targeted management led to clinical improvement, highlighting the need to consider hEDS/HSD in patients with intractable Long COVID symptoms. 3/
🔥 A landmark study challenges the long-held belief that Alzheimer’s disease (AD) is irreversible.
➡️ Using advanced mouse models that mimic human AD pathology, researchers found that restoring and maintaining healthy levels of NAD⁺, a key cellular energy molecule, can not only prevent but also reverse advanced Alzheimer’s pathology and fully restore cognitive function in mice. 1/
The team showed that NAD⁺ deficiency is a central driver of AD pathology—leading to blood-brain barrier breakdown, neuroinflammation, oxidative damage, and impaired neurogenesis. 2/
➡️ By administering a compound that rebalances NAD⁺ (P7C3-A20), all these pathological features were reversed, and memory and cognitive function were recovered.
➡️ These effects were seen in both amyloid-driven and tau-driven models, with supporting evidence from human AD brain samples suggesting disrupted NAD⁺ homeostasis in patients. 3/
As we age, our immune system becomes less effective, partly because key cells called CD8⁺ T-cells have trouble forming long-lasting memory.
A new study shows that a process called autophagy — the cell’s way of cleaning out old or damaged components — plays a central role in this problem. 1/
When a T-cell divides, it can make two daughter cells with different future roles: one becomes a long-lived ‘memory T cell’ that helps protect against future infections, and the other becomes a short-lived ‘effector T cell’ that fights the immediate infection.
For this to happen, the cell must sort its internal parts unevenly during division. 2/
The researchers found that #autophagy helps clear out old mitochondria before division, allowing daughter cells to inherit different mitochondrial content.
➡️ This asymmetric inheritance is crucial for creating a mix of T-cells with distinct fates — including memory cells.
➡️ Without autophagy, old mitochondria aren’t cleared, the inheritance becomes symmetric, and the diversity in T-cell fates is lost.
➡️ This has major implications for understanding why immune memory weakens with age and may inform new strategies to boost T-cell immunity. 3/
A new review highlights how neurotropic viruses like SARS-CoV-2 reprogram the metabolism of brain immune cells — especially microglia and astrocytes — contributing to neuroinflammation and brain dysfunction.
➡️ Under normal conditions, glial cells use oxidative phosphorylation (OXPHOS) to support brain homeostasis and anti-inflammatory functions. But viral infection shifts them toward aerobic glycolysis, driving pro-inflammatory cytokine production and immune activation. 1/
This metabolic switch:
• increases inflammatory mediators (IL-1β, TNF-α)
• elevates oxidative stress
• impairs neuronal support
• disrupts the blood-brain barrier
All of which can exacerbate neuroinflammation and damage. 2/
For SARS-CoV-2 specifically, the viral S1 protein can cross the BBB and trigger microglial activation and inflammasome (NLRP3) signaling, which further promotes inflammation and potentially persistent neurological effects. 3/
Breakthrough in respiratory virus prevention (Flu, COVID & more)
➡️ Researchers have developed an AI-designed intranasal antiviral platform that could block multiple respiratory viruses—flu, COVID-19, and future variants—right at the entry point: the nose. 1/
The platform is based on interferon-lambda, a natural antiviral protein, redesigned using AI protein engineering to overcome major limitations: poor heat stability and rapid clearance from nasal mucosa.
➡️ Using AI, scientists strengthened unstable protein regions, improved solubility, and added glycoengineering—making the protein so robust it remained stable for 2 weeks at 50 °C. 2/
To keep it in the nose longer, the protein was packaged in nanoliposomes and coated with chitosan, greatly improving adhesion to nasal mucosa and penetration through thick mucus. 3/
New study in International Journal of Infectious Diseases highlights persistent immune alterations after SARS-CoV-2 infection—providing further biological evidence for #LongCOVID as a genuine post-infectious condition.
➡️ Researchers found lasting changes in immune activation and regulation, even months after recovery from acute COVID-19—suggesting the immune system does not fully reset after infection. 1/
Key findings point to chronic inflammation, altered cytokine responses, and immune imbalance, which may explain prolonged symptoms such as fatigue, pain, and neurocognitive complaints.
➡️ Importantly, these immune changes were seen independent of initial disease severity, reinforcing that even mild COVID-19 can have long-term immunological consequences. 2/
The study of >40,000 people shows that key immune cells (T cells, B cells, NK cells) dropped during widespread COVID infection and stayed below pre-pandemic levels for nearly 2 years. 3/