We are organizing a coordinated research effort to revolutionize the diagnosis and treatment of #neuroinflammation illnesses and #mentalhealth symptoms.
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Mar 13 • 5 tweets • 2 min read
Traumatic brain injuries (TBIs) result in an immune response that can become dysregulated leading to neuroinflammation.
Could the first ever licensed treatment for TBI be a nasal spray? 🧵
Harvard scientists evaluated the efficacy of Foralumab in a mouse model of TBI.
This monoclonal antibody, which can bind CD3 and block T cell activation, is currently being tested in human clinical trials for treating MS and Alzheimer's.
Pro-inflammatory cytokines, like IL-1b, can cause the neurotoxic buildup of quinolinic acid (QUIN).
QUIN can cause cell death and neuroinflammation that triggers a never-ending loop of even more cell death and more neuroinflammation...🧵
But detecting QUIN in the brain is problematic due to inaccessibility and low concentrations.
That's why the QUIN precursor, kynurenic acid (KYNA), found in the blood is more routinely measured as a proxy for metabolic flux through this QUIN-producing biochemical pathway (the kynurenine pathway).
A surprising discovery finds a new mechanism that might explain the way beta-amyloid proteins accumulate in the Alzheimer's brain.
It could be the next big drug target for treating not only Alzheimer's but:
- Parkinson's
- Psoriasis
- Cancer
- Lupus
- etc.
🧵
\ The Discovery:
Researchers from the German Center for Neurodegenerative Diseases (DZNE) found that blocking the NLRP3 inflammasome enhanced the ability of immune cells in the brain (microglia) to phagocytose (eat) amyloid beta proteins.
This suggests that NLRP3 activation might contribute to amyloid beta plaque formation in Alzheimer's disease.
There is a multi-protein complex that plays a role in a vast number of diseases.
This includes, but is not limited to:
Amyotrophic lateral sclerosis (ALS)
Rheumatoid Arthritis
Sjögren’s
Alzheimer’s
Parkinson’s
Crohn's
Psoriasis
Epilepsy
Lupus
MS
Here is what it is and why there is a race to block it with a drug...🧵
\ Inflammasome:
The inflammasome is a multi-protein complex that (indirectly) activates the proinflammatory cytokines IL-1b and IL-18.
Many human diseases are characterized by high IL-1beta (IL-1b).
Significantly more than previously mentioned.
And blocking IL-1b can improve many disease outcomes.
But IL-1b and IL-18) are different than other pro-inflammatory cytokines...
Feb 14 • 6 tweets • 2 min read
Over 18 years ago a 26-year-old woman was admitted to the ICU due to inappropriate laughing, paranoia, and combative behavior (psychosis).
The medication she was given did not work and she fell into a coma.
The true cause of her condition led to the discovery of 10 brain diseases...🧵
Her only physical abnormalities, "were mild brain inflammation and a teratoma—a rare kind of germ cell tumor—in her ovary."
Dr. Josep Dalmau and his team began treating the woman with steroids and she soon recovered.
"It dawned on Dalmau that three other young women with similar symptoms referred to him in previous months also had benign ovarian teratomas."
Feb 7 • 7 tweets • 3 min read
Neuroinflammation is a hallmark of many conditions including, but not limited to:
- Autoimmune encephalitis
- Traumatic Brain Injury
- Long COVID
- ME/CFS
- MS
- etc.
A new discovery finds a gatekeeper of neuroinflammation below the skull ...🧵
Scientists from Harvard discovered that regulatory T cells (Tregs) between the skull and brain (meninges) act as gatekeepers preventing inflammatory immune cells from making interferon-gamma and entering the brain,
These Tregs also protect against inflammation-induced short-term memory loss.
In other words, these Tregs are like nightclub bouncers blocking entry into the brain.
But first, let's back up and explain what Tregs are...
A new NIH RECOVER study shows how surprisingly common it is for a SARS-CoV-2 infection to trigger ME/CFS...🧵
According to a new longitudinal study from the NIH RECOVER initiative, a SARS-CoV-2 infection increases your risk of developing ME/CFS by 393%.
Long COVID in adults is characterized by (protein) markers of:
- inflammation
- blood vessel clotting (thrombosis)
However, similar studies in pediatric cohorts are non-existent... until now.
The following confirms that pediatric Long COVID isn't a mental health condition...🧵
\ The Study:
Scientists from the University of Rome and Fondazione Policlinico Universitario discovered that 34 children and adolescents between the ages of 2 and 18 have an abundance of pro-inflammatory cytokines in their blood.
A subset of the cytokines have angiogenic (blood vessel growth-promoting) properties.
Jan 25 • 6 tweets • 2 min read
Certain gut bacteria are associated with major depressive disorder in a subset of people.
A new study might have discovered why...🧵
\ The Discovery:
Researchers at Harvard University found that the gut bacteria Morganella morganii enzyme mistakenly incorporates diethanolamine (DEA) into a lipid molecule.
DEA is a molecule found in:
- industrial products
- consumer products
- agricultural products
The DEA-containing lipid molecules are proinflammatory making IL-6.
Following a COVID infection, 25 y/o Angelica's heart would race.
“My heart started going insane."
"I could feel it pounding in my chest,” she recalled.
“I literally felt like I was going to die.”
This was her diagnosis...🧵
The diagnosis from numerous doctors was unanimous, "You have anxiety."
Angelic now bound to a wheelchair to prevent her racing heart responded in anger “...I have anxiety because of what’s happening to me.”
Jan 20 • 9 tweets • 2 min read
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...🧵
\ 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.
45% of those with Long COVID suffer from a sleep disorder (1).
It's so prevalent it's dubbed 'coronasomnia'.
Here is the science...🧵
\ 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.
Jan 16 • 7 tweets • 3 min read
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...🧵
\ 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.
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?
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.
Jan 4 • 10 tweets • 3 min read
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.
Dec 26, 2024 • 7 tweets • 2 min read
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.
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?
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.
Mutations in HLA are associated with many chronic diseases that impact the brain (and your mental health), including, but not limited to:
- Long COVID
- Sjogren's
- ME/CFS
- Lupus
- MS
- RA
Here is why in simple terms...🧵
\ Human Leukocyte Antigen (HLA):
HLA molecules arguably play the most important role in keeping you healthy.
That's because they act as molecular alarm systems in (almost) every cell in your body.