Post-COVID depression isn’t weakness.
It’s biology.
A landmark, important study shows how the virus leaves a measurable molecular trace - in the very proteins that protect your brain from degeneration🧵
It’s biology.
A landmark, important study shows how the virus leaves a measurable molecular trace - in the very proteins that protect your brain from degeneration🧵
https://twitter.com/atranscendedman/status/1976604964542873693
A new study in Translational Psychiatry shows that psychiatric symptoms after COVID-19 aren’t just psychological.
They have a biological signature - measurable changes in blood proteins linked to the brain, metabolism, and immunity.
They have a biological signature - measurable changes in blood proteins linked to the brain, metabolism, and immunity.
People who developed new depression, anxiety, PTSD, or insomnia after COVID showed distinct biochemical profiles compared to those who recovered fully or had other long COVID symptoms.
It’s not psychology.
It’s neurobiology.
It’s not psychology.
It’s neurobiology.
The key disruptions involve brain metabolism and immune inflammation.
Three major pathways were reflected in blood proteins.
Glucose metabolism (SORD, PKM)
Lipid metabolism (ApoA-II, ACOT7)
Cytoskeleton & membrane structure (Filamin A, VTA1)
Three major pathways were reflected in blood proteins.
Glucose metabolism (SORD, PKM)
Lipid metabolism (ApoA-II, ACOT7)
Cytoskeleton & membrane structure (Filamin A, VTA1)
The presence of α-synuclein in their blood suggests that SARS-CoV-2 can trigger neurodegenerative-like processes - misfolded proteins, microglial inflammation, and suppressed neuronal repair.
Interestingly, the nucleocapsid protein of SARS-CoV-2 can directly accelerate α-synuclein aggregation in vitro - basically mimicking the start of neurodegeneration.
Psychiatric symptoms may therefore be early neurobiological changes, not secondary psychological reactions.
Psychiatric symptoms may therefore be early neurobiological changes, not secondary psychological reactions.
Glucose metabolism.
Under stress or infection, the brain shifts into an energy-inefficient mode.
Reduced sorbitol dehydrogenase means sorbitol builds up - leading to oxidative stress and neuropathy, similar to diabetic nerve damage.
Under stress or infection, the brain shifts into an energy-inefficient mode.
Reduced sorbitol dehydrogenase means sorbitol builds up - leading to oxidative stress and neuropathy, similar to diabetic nerve damage.
Lipid metabolism.
ACOT7 helps neurons remove toxic fatty acids. Its alteration signals impaired detox and disrupted lipid homeostasis.
ApoA-II (part of HDL) is often reduced in Alzheimer’s and depression - a marker of low regeneration and weak anti-inflammatory defense.
ACOT7 helps neurons remove toxic fatty acids. Its alteration signals impaired detox and disrupted lipid homeostasis.
ApoA-II (part of HDL) is often reduced in Alzheimer’s and depression - a marker of low regeneration and weak anti-inflammatory defense.
Cytoskeleton & membranes.
Filamin A and VTA1 are linked to endothelial injury and neuroimmune dysfunction - findings also seen in long COVID and ME/CFS.
Filamin A and VTA1 are linked to endothelial injury and neuroimmune dysfunction - findings also seen in long COVID and ME/CFS.
Overall pattern.
Chronic neuroinflammation
Energetic exhaustion of neurons
Disrupted lipid protection (myelin, HDL)
Microvascular injury
A biological picture similar to neurodegenerative disease - but triggered post-infection.
Chronic neuroinflammation
Energetic exhaustion of neurons
Disrupted lipid protection (myelin, HDL)
Microvascular injury
A biological picture similar to neurodegenerative disease - but triggered post-infection.
These proteins could serve as biomarkers to identify people at risk of psychiatric sequelae after COVID.
And they can be detected from a single drop of blood - dried blood spot - cheap, repeatable, accessible.
And they can be detected from a single drop of blood - dried blood spot - cheap, repeatable, accessible.
That could transform care.
Helping doctors distinguish who needs neuroprotective or anti-inflammatory treatment, not just psychotherapy.
Helping doctors distinguish who needs neuroprotective or anti-inflammatory treatment, not just psychotherapy.
Sum:
After COVID-19, some people develop a biologically measurable neuroinflammatory phenotype.
It may look like depression or anxiety - but it’s really a reflection of immune and metabolic dysfunction in the brain.
After COVID-19, some people develop a biologically measurable neuroinflammatory phenotype.
It may look like depression or anxiety - but it’s really a reflection of immune and metabolic dysfunction in the brain.
This matters beyond adults.
If infection can reprogram brain metabolism and immune balance, the same mechanisms could affect developing brains too.
We urgently need to understand how post-COVID neuroinflammation shapes mental health trajectories in children and teens. @szupraha @ZdravkoOnline @adamvojtech86
If infection can reprogram brain metabolism and immune balance, the same mechanisms could affect developing brains too.
We urgently need to understand how post-COVID neuroinflammation shapes mental health trajectories in children and teens. @szupraha @ZdravkoOnline @adamvojtech86
It’s a warning sign that SARS-CoV-2 can disrupt brain balance in a way that closely resembles early neurodegenerative changes.
That doesn’t mean everyone will develop dementia - but it suggests the brain may enter a similar trajectory of inflammation and stress if these processes aren’t stabilized.
That doesn’t mean everyone will develop dementia - but it suggests the brain may enter a similar trajectory of inflammation and stress if these processes aren’t stabilized.
Baik at al., Discovery of molecular signature of long-term psychiatric sequelae in COVID-19 through proteome profiling of dried blood spots. nature.com/articles/s4139…
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