New study identifies 3 cognitive phenotypes in Long COVID - and raises a troubling question about insight and impairment.
123 adults
21 months post-COVID
All with some persistent cognitive complaints🧵
72% had objective cognitive impairment, mostly in attention and executive function
Using latent profile analysis, researchers identified 3 cognitive profiles:
Profile 1 (28%)
Broad, measurable cognitive deficits
Strong subjective complaints
High fatigue and functional impairment
Profile 2 (52%)
Milder but detectable deficits
Moderate subjective complaints
Weak correlation between symptoms and test results
And
Profile 3 (20%)
Primary deficit in verbal long-term memory
Few or no complaints in that specific domain
“They had impaired performance in the long-term verbal memory domain but reported few complaints.”
“This mismatch … might suggest anosognosia.”
Let’s be precise:
The main objective deficit in Profile 3 was in verbal long-term memory.
These participants still met inclusion criteria based on overall subjective complaints - but not in the domain where impairment was objectively detected.
This is not a case of global dysfunction - but a specific, unrecognized cognitive impairment.
Still, even such isolated deficits can affect everyday life:
- learning, communication, verbal recall, work efficiency.
Core finding: subjective complaints and objective impairment often don’t align.
Some felt impaired - and were
Some felt impaired - but weren’t
Some were impaired - but didn’t know it
This last group is especially concerning.
Authors conclude:
Long COVID-related cognitive dysfunction is heterogeneous
Self-report is insufficient
Brief screens (eg MoCA) may miss real impairment
Rehabilitation should be tailored to profile
Interpret cautiously - but take it seriously?
Even 21 months post-infection,
1 in 5 participants had measurable memory impairment - without realizing it. Something is missing - and they don’t know it.
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A new prospective cohort study (Nature Communications, 2025) followed 74,000 adults in Southern China and found - elevated EBV activity (measured by VCA-IgA) significantly increases the risk of several cancers.
First - limitations.🧵
Conducted in an NPC-endemic region with unique viral and population genetics
VCA-IgA was measured only once - no longitudinal antibody data
Lymphomas and other cancers were grouped, not stratified by subtype
Despite these limitations, this is one of the largest studies of its kind:
73,939 adults
Two independent cohorts
10 years of follow-up
Thousands of incident cancer cases tracked through registries
What actually helps people with ME/CFS and long COVID?
Not theory - but real-world data from 3,925 patients who rated over 150 treatments.
A new peer-reviewed study in PNAS (2025) analyzed what helped - and for which symptoms.
Here’s what patients report, symptom by symptom:🧵
Before we dive in - what do the percentages mean?
Patients reported whether a treatment helped a specific symptom (eg brain fog, fatigue).
So if a treatment shows 77% for brain fog, that means:
77% of patients who had brain fog and tried it said it helped.
It’s all self-reported
Brain fog
Top patient-reported treatments:
ADHD meds (methylphenidate, amphetamines) - 77% improved
Pacing (energy management) - 71%
IVIG (immunoglobulin) - 51%
Low-dose naltrexone (LDN) - 42%
Nattokinase/lumbrokinase - 50%
ADHD meds often worsen POTS - not for everyone
A new study in European Journal of Immunology (Mouton et al., 2025) followed hundreds of patients after COVID-19.
Their goal: understand why some people develop persistent symptoms - Long COVID / PASC.
The answer? T cells that never stand down.🧵
They followed over 450 people - both mild and severe COVID.
Findings:
40% of mild cases had PASC (sic)
57% of severe cases had PASC
But the key difference wasn’t viral load or inflammation.
It was how the immune system looked months later!
Blood tests showed:
No viral RNA
No spike protein in plasma
No strong systemic inflammation
But T cells told a different story:
The immune system was still on high alert.
Two years after a mild, non-hospitalized COVID infection, 1 in 10 people had measurable cognitive impairment.
They were younger. They never needed oxygen or ICU.
But they showed lasting deficits in memory, attention, or processing speed. COVID didn’t have to be severe to hurt your brain. Here’s what the new study found 🧵
A new study (Scientific Reports, 2025) followed 698 people from Matosinhos, Portugal:
COVID-positive and -negative
Hospitalized and non-hospitalized
All tested two years later with cognitive screening and full neuropsychological testing
The findings:
19.1% of patients hospitalized with COVID had cognitive impairment
10.7% of non-hospitalized COVID+ individuals
6.8% of hospitalized controls (no COVID)
3.2% of non-hospitalized controls.
COVID survivors were 3–5× more likely to show impairment.
Did you know SARS-CoV-2 uses the tetraspanin CD9 - the same membrane protein exploited by HIV - to infect human cells?
No, SARS-CoV-2 isn’t HIV.
But this surprising similarity reveals just how sophisticated this virus really is.
Let’s explore🧵
A new preprint (July 2025) shows that CD9 acts as a scaffold, gathering key entry factors SARS-CoV-2 needs:
ACE2 (main receptor)
NRP1 (boosts infectivity)
Furin and TMPRSS2 (spike-activating proteases)
CD9 clusters them at the membrane - like a viral docking station.
When researchers removed CD9 (via CRISPR) or blocked it with antibodies:
SARS-CoV-2 titers dropped 3–5×
NRP1 and ACE2 levels at the membrane fell
CD9 doesn’t just enable entry - it organizes and stabilizes the viral entry machinery!
COVID & Depression. A new study (Ogando et al., 2025) shows how residual SARS-CoV-2 in the brain may contribute to depression and anxiety in post-COVID condition (PCC).
The mechanism involves IL-6-induced activation of monoamine oxidase (MAO), which disrupts neurotransmitter balance.🧵
What do we know about PCC?
Post-COVID condition (PCC) affects 10–30% of infected individuals.
A majority (incl kids) experience CNS-related symptoms:
depression,
anxiety,
sleep disturbance,
cognitive dysfunction (brain fog).
But how do these arise?
This new study reconstructs a mechanistic pathway
Residual SARS-CoV-2 RNA is detected in the brain.
This leads to activation of microglia.
Activated microglia secrete IL-6.
IL-6 increases MAO-A and MAO-B expression and activity in glial cells.
MAO degrades monoamines such as serotonin, dopamine, and norepinephrine.
Disruption of monoaminergic signaling results in depressive and anxiety-like behavior.