Brie

🧠 Mostly RTing brain health and #longcovid stuff. Wishing you peace, health, and joy. Planetary and mitochondrial health.

[Brie @Brie_FI]

Site with Long Covid doctors you can filter. Some international. Displays Dr. specialties, trials, and publications. I have 1 filter in the screenshot, so there are more. DYOR re insurance, treatment protocols, etc.

https://t.co/R0IaXqBu4K

[Brie @Brie_FI]

@SmartAirFilters Interesting, I notice smoke from “just” trees triggers fewer symptoms than the constant soup of pollution in LA.

[Harry Spoelstra @HarrySpoelstra]

Blood–Brain Barrier Changes and Related Microvascular Outcomes in Long-COVID: A Comprehensive Review

🚨COVID doesn’t just infect the lungs, it leaves holes in the blood-brain barrier, a trail of microclots, inflammation, and lasting brain fog!

➡️This comprehensive USA/Brazilian review synthesizes evidence from 15 studies(2020-2025) on blood–brain barrier (BBB) disruption and microvascular injury in LongC0VID/PASC.

➡️Overview:
- SARSCoV2 drives systemic ENDOTHELIOPATHY,

- In vitro data show Spike protein causes direct endothelial toxicity, platelet aggregation, NF-κB activation, mitochondrial remodelling, and tight-junction (e.g., Claudin-5) downregulation,

- Animal models confirm structural BBB degradation, pericyte loss, and increased permeability (including with Delta/Omicron),

- Human clinical evidence reveals multifocal microthrombosis, elevated CSF/serum biomarkers of barrier leakage (QAlb elevated in ~50% of samples, total protein, S100B) and neuronal injury (NfL, GFAP), plus cytokine elevation (IL-6, IL-8),

- These changes facilitate neurotoxic influx (fibrinogen etc.), sustained neuroinflammation, impaired glymphatic clearance, and possible autoimmunity, without requiring detectable virus in CSF,

- Some BBB markers normalize over time yet symptoms persist, implying secondary cascades (hypoxia, inflammation) maintain LongC0VID phenotypes such as brain fog, fatigue, and cognitive deficits.

➡️Review conclusion:
“The evidence gathered in this review indicates BBB dysfunction as an important and multifaceted pathogenic mechanism in Long-COVID. We describe a continuous pathogenic cascade in which initial endothelial injury, driven by molecular imbalances, progresses to structural barrier collapse, thromboinflammation, and impaired glymphatic clearance. This sequence of events suggests that the clinical manifestations of cognitive decline and fatigue are not isolated neuronal deficits, but may be consequences of systemic vascular failure that alters the metabolic and homeostatic environment of the central nervous system.
Although the molecular pathways linking vascular injury to neurodegeneration are becoming increasingly clear, translating this knowledge into clinical practice remains a challenge. Furthermore, Long-COVID has demonstrated normalization of BBB markers without correlation with long-term symptoms, as observed in some reports, suggesting that other mechanisms are involved, underpinned by the consequences of the initial disruption rather than continuous leakage.”

‼️So, AGAIN, COVID-19 systematically damages cerebral ENDOTHELIUM and the BBB, creating a lasting vascular–inflammatory foundation for neurological LongC0VID. The population-level cerebrovascular risk remains elevated and demands urgent biomarker-validated, vascular-targeted therapies plus prospective studies.
Meanwhile: #AvoidSars2 #AvoidReinfections #StayVaccineUpdated
https://t.co/IrC2kwULOw

[Covid Institute @Covid_institute]

Researchers biopsied Long COVID muscle, exercised it until it triggered a crash, then biopsied the same muscle again. The "you're just deconditioned" story did not survive what they found. Thread on the study.

[Brandon Luu, MD @BrandonLuuMD]

Sleep deprivation makes people less willing to help others.

In this study, a single night without sleep reduced people’s desire to help, even friends.

At the societal level, donation amounts dropped ~10% after the spring daylight saving time sleep loss.

[Vipin M. Vashishtha @vipintukur]

⚡ A striking new clue to the mystery of Long COVID:

➡️ More than 80% of patients in this study showed evidence of central sensitization—a condition in which the brain and nervous system become hypersensitive, amplifying fatigue, pain, dizziness, brain fog, and other symptoms. 1/

[Jon Douglas @atranscendedman]

ADHD was linked to higher risk of COVID infection, worse acute illness, and long COVID.

The article frames this as a clue that ADHD is not just brain based, with immune and inflammatory pathways possibly involved.

https://t.co/FwoAdanK8S

[Harry Spoelstra @HarrySpoelstra]

Beyond brain fog: viral proteins as convergent drivers of neuroinflammation and proteinopathy

🚨“COVID-19 never really leaves your brain.”

New science review proposes SARSCoV2 viral proteins stay behind as long-lived toxins, triggering chronic neuroinflammation and planting the seeds of Alzheimer’s and Parkinson’s, even after mild infection.

This very interesting and eye-catching GERMAN review reframes post-viral neurological syndromes( L0ngC0vid) as driven by persistent viral proteins acting as long-term toxins ("protein-as-pathogen" model), not just the active infection!

➡️Core mechanisms:
- SARSCoV2 Spike and OTHER viral proteins activate glial TLR4/TLR2 receptors, triggering chronic neuroinflammatory cascades via NLRP3 inflammasome,
- They also disrupt autophagy, allowing toxic protein aggregates (tau, amyloid-beta, α-synuclein) to accumulate and seed neurodegeneration,

➡️SARSCoV2 specific evidence:
- Animal studies show Spike protein alone (without live virus) induces TLR4-mediated cognitive deficits, memory impairment, synaptic loss, and sustained neuroinflammation, recapitulating post-COVID syndrome,
- Spike binds α-synuclein, accelerating Parkinson-like clumps,

➡️Human data evidence:
- Millions experience "brain fog,"
- Post-COVID patients exhibit measurable brain damage: cortical thinning, hippocampal iron accumulation, and biomarkers of ongoing neuronal injury,

➡️Broader risks:
- Even mild infections leave lingering proteins that promote Alzheimer’s and Parkinson’s-like pathology via shared pathways,
- Same pathways seen in influenza, dengue, West Nile etc,
- Mild infection = no protection,

‼️So, according to this review, the “protein-as-pathogen” model makes it crystal clear: every new SARSCoV2 infection (even mild or asymptomatic) deposits more of these long-lived toxic viral proteins into the brain. They don’t fully clear. They accumulate.

Each reinfection reloads the TLR4/TLR2 → NLRP3 inflammasome trigger and further collapses autophagy, speeding up the tau/amyloid/α-synuclein proteinopathy and neurodegeneration.

SARS-CoV-2 does not just infect.

It weaponizes its own proteins as long-lived intracellular saboteurs.

Millions are probably already carrying this hidden payload.

This is not brain fog.

This is a silent, population-scale reprogramming of human brains toward dementia-like decline.

The long-term neurological cost will probably dwarf the acute pandemic itself!
#AvoidSars2 #AvoidReinfections
https://t.co/x0oxacaNwl

[Amy Mitchell @amymitchellart]

Same Christy. Though antivirals haven't fixed every related condition and symptom, my T and B cell counts have greatly improved. I no longer have lymphocytopenia.
The parallel can't be ignored: I'm successfully treating this new COVID Acquired Immune Deficiency with the same antivirals that treat HIV-AIDS.
Current combination is maraviroc, Stribild, Pemgarda, and Tollovid. Pemgarda is primarily for prevention in my case.

[Brie @Brie_FI]

It’s the new Long Covid cases for me

[Mike Hoerger, PhD MSCR MBA @michael_hoerger]

https://t.co/gNet1cxglI estimates 1.24 million infections per week in the U.S. during a "lull."

🧵2/5

[Brie @Brie_FI]

Bartonella or Babesia from fleas/ticks

[Brain Inflammation Collaborative @BrainInflCollab]

A recent study finds that 46% of people with ME/CFS were secretly infected with one of these two pathogens...🧵

[Danielle Beckman @DaniBeckman]

Is #LongCovid going away? Data show it is not. In a cohort study with 457.950 Covid cases, 1 in 6 patients developed Long Covid. Prevalence is 13-23% of US population, increasing 0.4%-1.5% every 3 months.
Cases remained stable through 2022 but started to increase in late 2023.

[Zdenek Vrozina @ZdenekVrozina]

Long COVID often does not appear in the system as long COVID.
Instead, the patient shows up
to primary care with fatigue,
to cardiology with dysautonomia or palpitations,
to endocrinology with a new metabolic problem,
to neurology with cognitive symptoms.

[Zdenek Vrozina @ZdenekVrozina]

The cumulative prevalence of PASC did not decline.
It slightly increased through mid-2024.
The authors interpret this as an accumulating burden, not just the fading tail of early pandemic waves.

[Prof. Akiko Iwasaki @VirusesImmunity]

Our new preprint by @peowenlu @SaefIzzy @weinerlabhms and colleagues shows that nasal anti-CD3 monoclonal antibody treatment can reduce neuroinflammation in a mouse model of Long COVID, even when administered at 4 weeks after infection 🧠
https://t.co/P8FZA2XA37

[Marco @Gmwetz]

„Researchers identified a two‑drug combination (dexmedetomidine + midodrine), called ACX‑02, that boosts the brain’s glymphatic waste‑clearance system“

I am wondering if this could help ME and LC patients ?

Especially for those who wake up unrefreshed or with a strong hangover feeling ?!

[Hannah Davis @ahandvanish]

Study of neuro #LongCovid patients found pTau-181 (marker of Alzheimer's/brain injury) increased by 59% after COVID.

Interestingly, levels increased more AFTER 1.5 years from infection (only 15% increased in the before-1.5 year time period).

https://t.co/QwEG1SwiOj 1/

[Bay Area Lyme Foundation @BayAreaLyme]

🚨 HUGE: A new pilot study found nearly HALF (46%) of MECFS patients tested positive for Bartonella or Babesia, stealth infections often missed by standard tests.

These treatable vector-borne pathogens (from ticks, fleas, cats, etc.) may be a force
driving the misery that often gets dismissed as “just fatigue.”

[Marco @Gmwetz]

Here is a good overview about the treatment in Japan for long COVID and post vac patients and the hypothesis around it ⬇️⬇️⬇️

You can send blood smear samples to see if you maybe could benefit from it.

[Neuroscience News @NeuroscienceNew]

For decades, “neuroinflammaging”, the slow-burning inflammation that causes brain fog and memory decline, was considered an unavoidable part of getting older. However, a landmark study suggests the clock can be turned back.

Researchers developed a non-invasive nasal spray that uses microscopic “delivery parcels” to travel directly into the brain. With just two doses, the therapy dramatically reduced chronic inflammation, recharged cellular “power plants” (mitochondria), and restored memory and cognitive sharpness in aging models.

https://t.co/XytygWNNZ2

#neuroscience #brain #science (1/3)