New meta-analysis - SARS-CoV-2 leaves long-lasting neurological damage in millions.
This isn’t rare. Not "just stress."
It’s a massive biological hit to the brain - with consequences for the whole society.🧵
125 studies, over 4 million people, ≥6 months post-infection.
Prevalence of key symptoms:
Memory problems 27.8%
Cognitive impairment 27.1%
Sleep disorders 24.4%
Attention issues 23.8%
Fatigue 43.3% ...
Many with mild outpatient COVID report persistent cognitive problems.
The brain is systematically affected across the full spectrum of disease severity.
This meta-analysis doesn’t present a new biological mechanism.
Its value is different:
It shows how widespread this damage is
It quantifies the population-level impact
It turns scattered evidence into hard numbers
Neuroinflammation, microvascular injury, BBB dysfunction - these are known.
What’s new here:
How common and persistent these brain-related symptoms are.
This isn’t a rare complication.
It’s a systemic crisis.
Brain dysfunction isn't just a personal tragedy.
It’s a societal vulnerability:
Reduced productivity
Learning difficulties
Impaired relationships
Key professions under pressure (healthcare, education)
The brain is just the visible tip of the iceberg.
When cognition fails, you notice.
But underneath may lie next immune, vascular, and metabolic injury.
Neurological symptoms are a signal of deeper biological disruption.
And if we don’t take it seriously, it will keep eroding our collective capacity @szupraha @ZdravkoOnline
Elboraay et al., 2025, Long-term neurological and cognitive impact of COVID-19: a systematic review and meta-analysis in over 4 million patients bmcneurol.biomedcentral.com/articles/10.11…
• • •
Missing some Tweet in this thread? You can try to
force a refresh
Targeting DNA sensors isn’t exclusive to DNA viruses.
Even RNA viruses - which don’t carry any DNA - have evolved ways to silence the same intracellular alarm: cGAS–STING.
This is convergent evolution in action: different viruses, different tricks, same target. @dbdugger 🧵
The sensor cGAS sounds the alarm when it detects DNA in the wrong place - the cytoplasm.
That DNA might come from:
a DNA virus
or even from our own cell (eg leaked mitochondrial or nuclear DNA during stress)
When cGAS is activated, it produces cGAMP, which triggers interferons - our antiviral sirens.
So if a virus wants to stay hidden early in infection, it must avoid or disable this DNA sensing.
A new preprint (June 2025) shows that microclots formed during COVID-19 can obstruct capillaries and impair microcirculation.
And remarkably, an earlier peer-reviewed study reached the same conclusion - by a completely different method. 🧵
In the new study by Kell, Pretorius et al., SARS-CoV-2 is associated with abnormal blood clotting that produces fibrinaloid microclots - clots containing amyloid (!) fibrin that are resistant to fibrinolysis (breakdown). preprints.org/manuscript/202…
These microclots are made of amyloid-type fibrin - a misfolded version that resists not only natural fibrinolysis, but also standard clot-busting drugs.
In other words: your body can’t easily remove them. Neither can your meds.
Persistent virus = persistent symptoms. New peer-reviewed data confirm - long COVID patients still carry spike protein fragments - and show signs of immune breakdown.
What’s left behind doesn’t stay silent.🧵
This 2025 study analyzed blood samples from 65 patients with post-COVID condition (PCC, aka long COVID).
All had been infected between 2020 and mid-2021, before Omicron.
Using targeted mass spectrometry (MRM/SRM), researchers detected SARS-CoV-2 spike and nucleocapsid (NCAP) proteins in the plasma of symptomatic PCC patients.
These viral proteins persisted even 3–5 years after infection (sic) - but were absent in recovered, asymptomatic individuals.
New brain MRI study (2025): Post-COVID patients show measurable structural changes - even without hospitalization.
Participants were not selected for having Long COVID!
What was found, why it matters, and how this fits into what we know about hypothalamus-related circuits. 🧵
COVID-19 doesn’t always leave visible scars - but in the brain, it leaves measurable traces.
A new multimodal MRI study (N=76 post-COVID vs N=51 controls) shows focal loss in key subcortical and limbic areas.
That includes:
Right amygdala, hippocampus, thalamus
Right putamen, caudate, pallidum
These aren’t random.
They’re deep grey structures involved in motivation, memory, alertness - all connected with hypothalamus-mediated homeostasis.
Aspirin and post-COVID diabetes:
A new large cohort study (35,000+ participants) found that daily low-dose aspirin reduces the risk of developing type 2 diabetes by 52%.
What exactly did they find? And why does this underscore the role of inflammation in COVID aftermaths?🧵
Researchers followed 35,525 adults in Italy from 2018 to 2022.
Main question: does daily low-dose aspirin (100 mg) reduce the incidence of new-onset type 2 diabetes (T2D)?
They used propensity score matching to balance age, BMI, prediabetes, and medications between groups.
Results:
Aspirin reduced the risk of T2D by 52% overall (HR = 0.48)
By 29% pre-pandemic
By 62% during the COVID-19 pandemic
The more systemic inflammation (eg COVID), the greater the benefit.
Lockdowns hurt children.
We hear it all the time.
But this study shows that COVID-19 infection itself - not just pandemic stress - biologically drives serious mental health risks in kids.
Among 180k children, COVID was linked to:
suicidality
self-harm
poisoning🧵
Researchers analyzed Utah health insurance data from 2019-2021.
They compared kids (6-15) with and without confirmed COVID-19.
Children who had COVID showed:
2× higher risk of suicidal ideation
2.05× higher risk of self-harm
2.21× higher risk of poisoning (eg medication overdose)
And for those who had severe COVID:
Suicidal ideation: 2.53× higher
Self-harm: 2.57× higher
Poisoning: 2.68× higher
This wasn't about anxiety or school closure.
This was a dose-response pattern: more severe infection - more serious outcomes.