COVID can damage memory - even months after recovery.
Not just any memory: the precision of memory, tied to the hippocampus.
A new study shows that it doesn’t recover over time!
It actually gets worse.
A short thread on the hippocampus, neurogenesis, and a virus that lingers.🧵
The hippocampus isn’t just - a memory disk.
It’s one of the only brain areas where new neurons grow in adulthood!
It helps us:
learn new things
navigate space and time
distinguish between “same” and “similar”
Exactly what “brain fog” disrupts.
A new study (Meyer & Zaiser, 2025) tested >1400 people using a memory precision task.
People post-COVID showed significantly lower scores (LDI).
The deficit appeared even in those who felt fully recovered!
This wasn’t fatigue or depression.
It was hippocampal dysfunction.
The most concerning finding?
The longer since infection, the worse the result.
Memory didn’t improve - it declined.
This suggests:
persistent neuroinflammation,
or
a slow, degenerative process.
Memory isn’t just about “how much” you remember.
It’s about how precisely your brain can separate similar events.
Losing that ability means:
poor decisions
impaired learning
mental exhaustion
Often without being aware of it.
The hippocampus is a silent but essential player.
COVID can disrupt its function even without severe illness.
And time alone may not heal it.
Worse: the process may slowly continue.
What do other studies show?
Post-mortem findings in COVID-19 patients:
fewer new neurons in the dentate gyrus
activated microglia
elevated CCL11 - a known blocker of neurogenesis
Animal models:
loss of newborn neurons
memory deficits
behavioral changes
We don’t yet know how long the neurogenesis block lasts.
But we do know:
it can persist for months or more
and may take on degenerative features in some people
In a chronically inflamed hippocampus, new neurons may be completely suppressed.
Sound familiar?
Some HIV’s proteins (Tat, gp120) - hippocampal inflammation, loss of neurogenesis, cognitive decline.
SARS-CoV-2? Spike, ORF3a, N, E.
Different virus, same target.
Long COVID isn’t just “feeling tired.”
It’s a measurable, inflammatory brain syndrome.
And the hippocampus may be one of its first victims.
Meyer & Zaiser, 2025, Insights on the neurocognitive mechanisms underlying hippocampus-dependent memory impairment in COVID-19 nature.com/articles/s4159…
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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.
COVID turns common EBV reactivation into a clinically significant event.
A new Czech study (Cell Reports, 2025):
SARS-CoV-2 can trigger Epstein-Barr virus (EBV) reactivation - and in some people, that leads to long-term lung damage in long COVID.🧵
The study analyzed 687 people with long COVID (4–16 weeks after infection).
Tests included:
lung function & chest X-ray
EBV serology (VCA IgM, IgA, EA-D IgG)
EBV DNA in blood
IL1/IL10 genetics
cytokines & immune profiling
Signs of recent EBV reactivation were found in 23% of patients.
Key marker: anti-VCA IgA
This antibody:
indicates a strong, recent EBV reactivation
correlates with lung damage and higher EBV viral load in blood
A major new review from Yale (Moen, Baker, Iwasaki, 2025) offers the most comprehensive picture yet of what SARS-CoV-2 does to the nervous system.
The conclusion is stark:
Long COVID is a chronic neuroimmune disorder affecting brain, spinal cord, and peripheral nerves.🧵
Warning Sign #1: The pandemic didn’t end - it just changed shape.
The virus keeps evolving. The acute symptoms may fade.
But for many, the infection never truly ends.
Even young, previously healthy people experience:
mental fog,
dizziness when standing,
sensory disturbances,
exhaustion after minimal effort,
racing heart.
That’s Long COVID.
Warning Sign #2: The virus leaves behind molecular debris - and the immune system won’t let it go.
Sometimes it’s spike protein fragments in the blood.
Sometimes viral RNA in the olfactory bulb or even the skull.
This triggers persistent immune alarms:
T cells get activated
Inflammation spreads to the brain
Neuronal connections start breaking down
The war continues - long after the virus is gone.
A new 2025 preprint confirms: Long COVID (PCS) is biologically real - and it’s in the brain.
The key culprit? Chronic, low-grade neuroinflammation.
It can persist for months or even years.
Here why it matters 👇
What is PCS (Post-COVID Syndrome)?
Not “just anxiety.
Not “just fatigue.”
It’s a state of ongoing immune activity in the brain after SARS-CoV-2 infection!
Common symptoms:
brain fog
fatigue
anxiety
sleep disturbances
memory loss
What drives brain inflammation?
This study identifies 9 key mechanisms keeping it alive:
spike protein persisting in brain/skull
chronic glial activation
blood-brain barrier (BBB) disruption
autoimmunity
viral reactivation (EBV, HERVs)
microclots & hypoxia
vagus nerve dysregulation
mast cell activation
histamine system abnormalities
What connects HIV and SARS-CoV-2 in the brain?
Not structural homology - but functional parallels between viral proteins that can drive chronic neuroinflammation and immune evasion.
A short thread on Tat, viroporins, ORF8, and viral neuropathogenesis. @dbdugger 🧵
COVID-19 (Long COVID) is associated with:
microglial activation
blood-brain barrier (BBB) disruption
persistent viral antigens
memory and attention deficits
These are also key features of HIV-associated neurocognitive disorder (HAND). What’s the link?
In HIV, the Tat protein is central to neuropathology:
secreted from infected cells
crosses the BBB
activates microglia via TLR4
triggers IL-6, TNFa, ROS
promotes excitotoxicity in neurons
Tat = neurotoxic transcriptional regulator.
In recent months, a growing number of robust scientific studies have confirmed that even mild SARS-CoV-2 infection is not biologically neutral in children. Two new studies reveal surprising depth of impact - metabolically and immunologically.🧵
For years, pediatric COVID-19 was framed as "mild."
But a large metabolomic study (Lawler et al., 2025) shows that even children with mild symptoms show significant systemic changes in their blood - and a newer study (Gaebler et al., 2025) suggests some of these changes persist.
Lawler et al. analyzed 147 children
55 had acute COVID-19 (most were not severely ill)