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...🧵
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.
Committed to exploring all immunological causes of her condition, Alina traveled to see Ludger Tebartz van Elst, a neuropsychiatrist at the Albert Ludwig University of Freiburg in Germany specializing in identifying and treating autoantibodies that attack the brain.
After a thorough examination, Dr. Tebartz van Elst found autoantibodies in her blood that target a brain protein called contactin-associated protein-like 2 (CASPR2).
CASPR2 is found in the CNS and is crucial to the transmission of neural signals.
Alina was treated with intravenous cortisone and she, "got [her] life back” almost immediately.
Alina could jog a few days after treatment for the first time in nearly a decade.
This is one of many stories revealing how a subset of patients suffering from psychosis, chronic fatigue, memory loss, etc. have autoantibodies in their blood that are attacking the brain.
These autoantibodies are commonly formed in response to a herpes infection in the brain or a tumor.
We at the Brain Inflammation Collaborative are dedicated to educating the masses that the immune system can change how we think, feel, and act causing an array of neuroimmune axis diseases and psychiatric conditions.
If you want to support our efforts please give this post a like and share it with your social networks!
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50% of long COVID patients had this virus in their oral mucosa.
It might contribute to the pathology of Long COVID.
Here is why...🧵
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?
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
There is an emerging field of medicine called Immunopsychiatry.
Immunopsychiatry requires the combined effort of immunologists, neurobiologists, neuroimaging specialists, and psychiatrists...🧵
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!
Anti-depressants don't work for 30% of people who take them.
This study might have discovered why...🧵
\ The Discovery:
Scientists at the Imperial College of London and the University of South Carolina discovered that an inflammatory molecule called histamine directly inhibited the release of serotonin in the brain of mice.
\ Histamines:
Histamines are molecules produced by mast cells that cause the typical symptoms associated with allergies such as:
- watery eyes
- runny nose
- sneezing
- itching
Histamines can also be released in the brain by mast cells and some neurons.
Autoantibodies can cause psychosis-like conditions characterized by a disconnection from reality, often involving:
- delusions
- hallucinations
- impaired thinking or reasoning.
A subset of these cases are actually caused by a rogue immune response...🧵
🧠 Psychosis And Autoantibodies:
Up to 10% of psychosis patients have been reported to contain an autoantibody called anti-NMDAR that targets the brain causing autoimmune encephalitis (AE) (autoantibody-driven brain inflammation) (1).
However, only 18 harmful brain autoantibodies are known to science (2). What if there are more?
➡️ The Problem:
If the immune system of a psychosis patient makes a brain-reactive autoantibody unknown to science then that patient will have to suffer in silence... until now.
Immune cells can 'talk' to neurons and vice versa.
Abnormal communication between these cell types is found in:
- PANDAS/PANS
- Long COVID
- Depression
- ME/CFS
- PTSD
- etc.
A new study discovered how...🧵
\ The Discovery:
Scientists discovered that a subpopulation of neurons expresses a cytokine receptor, allowing them to sense and respond to inflammation.
The receptor, called neuronal IL-1RI (nIL-1R for short), changed the behavior of neurons following IL-1 stimulation.
Here we will explain the significance in simple terms.