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Jan 18 β€’ 10 tweets β€’ 3 min read β€’ Read on X
45% of those with Long COVID suffer from a sleep disorder (1).

It's so prevalent it's dubbed 'coronasomnia'.

Here is the science...🧡 Image
\ Coronasomnia:
There is a strong association between Long COVID and the development of:
- insomnia
- sleep continuity disorders
- feeling of non-restorative sleep
- changes in the sleep-waking cycle

However, this is not unique to Long COVID.
\ Sleep and ME/CFS:
Those with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and other neuroinflammatory conditions also have similar disordered sleeping patterns (2).

This debilitating condition is symptomatically similar to Long COVID.

Like long COVID, it can also be triggered by a pathogen such as:
- Borrelia burgdorferi (Lyme disease)
- Epstein-Barr Virus
- Herpesvirus 6
- Influenza
- etc.
\ Hypothalamus Infection:
Why might these chronic sleep issues exist?

The SARS-CoV-2 virus has been identified in the hypothalamus in those with acute COVID-19 (3).

The hypothalamus not only regulates our sleep but also our:
- stress response (HPA axis)
- cardiovascular function
- body temperature
- metabolism
- respiration
\ The Hypothalamus and Sleep:
The development of sleep disorders might be explained by SARS-CoV-2 infecting neurons in the hypothalamus.

It's suggested the virus infects the hypothalamus by entering the olfactory bulb in the nasal cavity (pictured below). Image
\ Orexin
Specifically, specialized hypothalamic neurons make orexin a molecule that regulates sleep-wake cycles (4).

These neurons are particularly susceptible to infections and can die and never regenerate.
\ Inflammation and Orexin:
Neuroinflammatory and neurodegenerative diseases have been found to reduce orexin levels (5).

This is associated with:
- narcolepsy
- fragmented sleep
- REM sleep dysregulation
There is more to the story but it's too much information to put in this thread.

Instead, we wrote a deep dive to help you understand the relationship between poor sleep and neuroinflammation.

Inside you'll find
- how neuroinflammation affects sleep hormones
- sleep-promoting medications
- circadian rhythm
- and more

Link πŸ‘‡
buff.ly/4fYCopy
We at the Brain Inflammation Collaborative are on a mission to help researchers understand how complex neuroimmune axis diseases impact our brain health and mental health.

If you found this informative please give it a like and share!
Literature Cited:
1. Cinthya Pena-Orbea, et al. J Gen Intern Med. June 2023. PMID: 37014604
2. A FerrΓ©. Neurologia. PMID: 26877195
3. Agrawal, S. et al. Acta Neuropathol Commun. Dec 2022. PMID: 36528671
4. Abdelmissih, S. et al. Cureus. Oct 2022. PMID: 36457603
5. Berhe DF, Gebre AK, Assefa BT. Pharmacology Biochemistry and Behavior. PMID: 32315694

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More from @BrainInflCollab

Jan 20
Muscle weakness is one symptom of post-exertional malaise (PEM).

This is experienced by those with:
1. Long COVID
2. ME/CFS
3. TBI
4. MS

Data suggests this is to blame...🧡 Image
\ The Discovery:
Scientists at Washington University in St Louis discovered that neuroinflammation causes neurons to make IL-6.

The IL-6 communicates with skeletal muscles to cause profound muscle fatigue.

Here is how...

Read the full study πŸ‘‡
buff.ly/4jnaAxN
\ The Methods:
3 different CNS stressors were used to cause neuroinflammation in πŸ€ :
- Neuronal expression of a SARS-CoV-2 gene (ORF3a) in the brain
- E. coli infection of the brain
- An Alzheimer's πŸ€ model
Read 9 tweets
Jan 16
Suicide is thought of as an extreme moment of despair followed by voluntary loss of life in an otherwise healthy individual.

However, research suggests neuroinflammation is to blame.

Here is the science in simple terms...🧡 Image
\ The Discovery:
Scientists studied the brains of 29 diseased suicide victims (and 31 controls).

They found that neuroinflammation disrupted the brain's balance between inhibitory and excitatory neuronal signaling.

Read more:
buff.ly/3uoj4A5Image
Specifically, scientists found:
- More excitotoxicity - an inflammatory process that can lead to cell death.
- A gene called NPAS4 was significantly reduced in the suicide brain cohort.

What is NPAS4?
NPAS4 is a protein that turns 'on' genes involved in:
- development of inhibitory synapses (balancing neuron firing)

Here is what that means in simple terms...
Read 7 tweets
Jan 10
50% of long COVID patients had this virus in their oral mucosa.

It might contribute to the pathology of Long COVID.

Here is why...🧡 Image
Significantly more Epstein-Barr virus (EBV) was detected in Long COVID patients compared to healthy COVID-recovered patients (15/30 LC vs 4/20 non-LC controls).

A similar independent study (1) can to the same conclusion.

This is important because EBV reactivation is highly pathogenic as it's associated with:
- Rheumatoid arthritis
- Sjorgrens syndrome
- Multiple sclerosis
- Type 1 diabetes
- Celiac disease
- Some cancers
- ME/CFS
- Lupus

Could a subset of Long COVID cases be attributed to the inability to block EBV reactivation?

Read more:
buff.ly/4jawbtc
\ EBV Background:
Once you become infected with EBV you're infected for life.

Symptomatic infection can cause mononucleosis but, significantly more people become asymptomatically infected with EBV.

In fact, it's estimated that 95% of the world's adult population is Epstein-Barr virus (EBV) positive (2).
Read 10 tweets
Jan 8
In 2017 Alina Sternberg, a psychiatrist, was hit with crushing fatigue and brain fog.

Neurologists told her the symptoms were caused by depression.

"No, I can enjoy my life and I know what depression is... I’m a psychiatrist!”

It took another 6 years to discover the culprit...🧡Image
Alina's symptoms became progressively worse.

By 2023 she spent most of her days in bed.

Not only was she hit with soul-crushing fatigue but her memory deteriorated.

One day she forgot her way home, a place she had lived for 20 years.
Alina asked a colleague at the hospital where she worked if he would check to see if she had autoantibodies in her blood that might be attacking her brain.

He told her, "That is impossible because you aren't psychotic.”

Other neurologists agreed.
Read 8 tweets
Jan 4
The SARS-CoV-2 spike protein was recently found to localize in an unusual place outside the brain.

This localization pattern might explain the neuroinflammatory symptoms experienced during:
- SARS-CoV-2 infection
- Long COVID..🧡
Researchers from Ludwig-Maximilians-University Munich, Munich, Germany found that the SARS-CoV-2 spike protein localizes to the skull's bone marrow.

To understand why this discovery is important in the context of Long COVID we must first learn about the following:
- the meninges
- immune cells in the meninges

Read the scientific publication here:
buff.ly/3DNfPGLImage
\ Background - Skull Meninges Connections (SMCs):
The brain is wrapped in a 3-layer membrane called the meninges.

This protective membrane contains resident immune cells that do not come from circulation.

Instead, they traffic through specialized channels from the skull's bone marrow (to the meninges) (1).Image
Read 10 tweets
Jan 1
There is an emerging field of medicine called Immunopsychiatry.

Immunopsychiatry requires the combined effort of immunologists, neurobiologists, neuroimaging specialists, and psychiatrists...🧡 Image
This growing field of psychiatry challenges the traditional ways psychiatrists view the cause of mental illness.

Instead of faulty neuronal signaling causing depression or anxiety immunopsychiatrists examine the role of immune processes in controlling our mental health.
We envision a world where ALL the causes of mental illness are widely understood and promptly diagnosed and treated.

Help make our vision a reality by liking and sharing this content!

Read more about immunopsychiatry here: buff.ly/4gzPt9W
Read 4 tweets

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