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Memory and Autoimmune Encephalitis

Memory and Autoimmune Encephalitis

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January 24, 2024 | by Ryan Rahman, PennNeuroKnow and IAES Collaboration

A message from IAES Blog Staff:

The staff at IAES is proud to present to all of you another wonderful article/blog from the amazing team at PennNeuroKnow. Since 2019 IAES has been extremely lucky to be in partnership with the PennNeuroKnow(PNK) team to help us all better understand complex medical issues related to AE and neurology in general. The talented PNK team continues to keep us up-to-date and help clarify the complexities we face each day along our AE journey, and we are eternally grateful! You can find out much more about this stellar group at: https://pennneuroknow.com/

—-

Introduction

Our brains are what make us human – consciousness, emotion, and memory all come from a tapestry of over 100 trillion connections. When this intricate network is bombarded by misguided immune cells, as in the case of autoimmune encephalitis, the brain can no longer carry out some of its most important functions. One such function that is often prominently affected is memory.1,2 Memory is a central aspect of our daily lives, allowing us to recall cherished moments, learn from our experiences, and navigate the world. However, for individuals battling autoimmune encephalitis, memory can become a complex and challenging puzzle. In this blog post, we will describe the memory difficulties patients face when living with autoimmune encephalitis (AE).

What is memory?

Memory is a fundamental cognitive function that enables individuals to absorb, store, and recall information and experiences. It plays a crucial role in shaping our perception of the world and our ability to learn, make decisions, and navigate daily life. There are different types of memory that work together to enable us to learn, adapt, and navigate the complexities of life. Broadly, it can be helpful to think of grouping different types of memory by where they are in the brain because the brain organizes its functions into different locations. For example, the hippocampus is the main brain structure that helps record information and start the formation of memories.3 In addition, it is also important to consider the kind of information being stored and how long it is stored for (Figure 1). Here, we break down a few types of memory that are relevant to patients living with AE:

Sensory Memory: Sensory memory4 is responsible for briefly holding information from our sensory organs, such as vision and hearing. This short-lived memory lasts for a fraction of a second and is composed of all the information we get from our senses before our brain filters out the unimportant parts. It typically relies on parts of the brain that receive direct information from the sensory organs, such as the eyes and ears.

Short-Term Memory: Short-term memory4 is the next shortest type of memory, lasting for a few seconds to minutes. When you solve a quick math equation in your head or remember mid-conversation what someone just told you, you’re using your short-term memory.6 Short-term memory relies largely on communication between two parts of the brain called the prefrontal cortex and hippocampus.

Long-Term Memory (LTM): Long-term memory4 is exactly what it sounds like – the kind of memory that helps us remember things for long periods of time. It has an almost unlimited capacity and can last for a lifetime. Long-term memory includes our ability to remember personal experiences, facts, skills, and habits. Our ability to form these memories relies on the hippocampus and another part of the brain called the frontotemporal lobes, but where exactly long-term memory is stored is still unclear.

Procedural Memory: Procedural memory4 is a special type of long-term memory often mistakenly called “muscle memory” (because memory comes from the brain, of course!) that allows us to ride a bicycle, type on a keyboard, or tie our shoelaces with little conscious effort. Procedural memory does not depend on the hippocampus or prefrontal cortex. Instead, it tends to be formed and stored in the brain areas involved in planning motions, such as the cerebellum and the motor cortex.

Because different types of memory rely on different parts of the brain, sometimes patients with damage to only some parts of the brain can have deficits in only one type of memory, while the other types of memory are preserved.

Another concept that is central to most types of memory is the idea that brain cells, which are called neurons, can change the strength of their connections. Connections between neurons are called synapses, which are tiny gaps between the cells bridged by chemical and electrical signals.5 A bunch of neurons working together can mirror an electrical circuit, and the more synapses in a circuit are activated, the tighter and more numerous these connections become. This concept is known as synaptic plasticity, and the ability to retrieve memories may be dependent on how strong certain connections are.6

memory 1 - Memory and Autoimmune Encephalitis

Figure 1. Memories form in discrete steps over time and are associated with specific parts of the brain.

 

How does autoimmune encephalitis affect memory?

Over the course of many years and research studies, doctors and scientists have shown that AE causes changes in memory. Both short-term and long-term memory impairments can occur in patients with AE; however, procedural memory impairments do not usually occur in AE.1,7-9 For patients with AE, deficits in short term memory can take the form of confusion and attention challenges; whereas deficits in long term memory can take the form of difficulty remembering facts, struggles with planning/organizing, and loss of personal memories. Although many patients show significant improvement in their memory symptoms after treatment of AE, many patients can unfortunately continue to experience residual memory problems, even long after other symptoms of AE have gone away.10

As discussed in a prior IAES blog post, AE is divided into different types based on which brain protein is attacked by a patient’s immune system. People with some subtypes of AE are more likely to have certain memory challenges.11 For example, patients with LGI1 autoimmune encephalitis (patients who have antibodies against Leucine-rich Glioma Inactivated protein 1) tend to have the most severe memory deficits with a profound loss of memories about personal life events. In contrast, memory loss and confusion are less common in patients with GABAAR encephalitis (~27%) and GABABR encephalitis (~47%). The reason behind these differences may in part be due to the fact that some of these proteins are only present in specific parts of the brain, which, as we previously discussed, control specific types of memory. Additionally, these targeted proteins play different roles in the circuits of the brain and disruption of different parts may impair synaptic plasticity in various ways. Please see the table below for more details about the memory changes experienced in different types of AE.

antibodies - Memory and Autoimmune Encephalitis

Table 1. Different types of AE are associated with different memory challenges for patients. Adapted from Gibson et al. – Cognitive impact of neuronal antibodies: encephalitis and beyond (2020).

 

To understand more about how AE causes memory changes, scientists first worked with patients using magnetic resonance imaging (MRI) to look at changes in the physical structure of their brains.12 Even as early as 1968, scientists saw drastic changes in the temporal lobes of patients with AE, which is a large region of the brain that contains the hippocampus.13 Importantly, recent studies have directly demonstrated that most patients with autoimmune encephalitis have structural changes in the hippocampus, and those with more damage in the hippocampus have more severe challenges with memory.14  

In addition to large structural changes, the microscopic science behind how AE causes memory loss has been explored in animal studies, which are more manipulable models for scientists to determine how diseases work in an entire system.15,16 In one experiment, scientists injected mice with antibodies from human patients with AE. They then tested the mice for any memory changes. Mice that were given the AE-associated antibodies could not remember objects they had seen before and developed anxiety-like behaviors.15 Importantly, scientists also showed that antibodies targeting the Nmethyl-Daspartate (NMDA) glutamate receptor (as seen in patients with Anti-NMDAR encephalitis) reduced the number of these proteins at the connections between brain cells which in turn disrupted synaptic plasticity.16

As previously mentioned, synaptic plasticity refers to the dynamic strength of circuits in the brain which increases when more neurons are activated together. Since glutamate is the main activating signal of the brain, it may be that destruction of the glutamate signal in certain types of AE leads to impaired memory by changing the strength of connections in the brain.

Lastly, an exciting early development occurred when scientists discovered that injecting Ephrin-B2, a protein that helps in the development of connections in the brain, was able to prevent memory loss caused by anti-NMDA antibodies in mice.16,17 Based on these findings, Ephrin-B2 may one day become a potential treatment for memory loss in patients living with AE!

Conclusion

In conclusion, autoimmune encephalitis is a neurological disorder that can have a profound and lasting impact on memory. Memory deficits in autoimmune encephalitis are not only distressing for patients but can also pose challenges to their daily functioning and quality of life. A better understanding of the mechanisms underlying these memory impairments and the development of targeted treatments are crucial to improving outcomes for individuals affected by autoimmune encephalitis and their memory-related challenges.

 Research in this field is ongoing, and with continued advancements in science and treatment, we can piece back together the lives of those affected by autoimmune encephalitis, one memory at a time.

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References

1          Heine, J. et al. Long‐Term Cognitive Outcome in Anti–N‐Methyl‐D‐Aspartate Receptor Encephalitis. Annals of Neurology 90, 949-961 (2021). https://doi.org/10.1002/ana.26241

2          McKeon, G. L. et al. Cognitive outcomes following anti-N-methyl-D-aspartate receptor encephalitis: A systematic review. Journal of Clinical and Experimental Neuropsychology 40, 234-252 (2018). https://doi.org/10.1080/13803395.2017.1329408

3          Bird, C. M. & Burgess, N. The hippocampus and memory: insights from spatial processing. Nature Reviews Neuroscience 9, 182-194 (2008). https://doi.org/10.1038/nrn2335

4          Camina, E. & Güell, F. The Neuroanatomical, Neurophysiological and Psychological Basis of Memory: Current Models and Their Origins. Front Pharmacol 8, 438 (2017). https://doi.org/10.3389/fphar.2017.00438

5          Südhof, T. C. & Malenka, R. C. Understanding Synapses: Past, Present, and Future. Neuron 60, 469-476 (2008). https://doi.org/10.1016/j.neuron.2008.10.011

6          Citri, A. & Malenka, R. C. Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms. Neuropsychopharmacology 33, 18-41 (2008). https://doi.org/10.1038/sj.npp.1301559

7          Dalmau, J. et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol 7, 1091-1098 (2008). https://doi.org/10.1016/s1474-4422(08)70224-2

8          Finke, C. et al. Cognitive deficits following anti-NMDA receptor encephalitis. Journal of Neurology, Neurosurgery & Psychiatry 83, 195-198 (2012). https://doi.org/10.1136/jnnp-2011-300411

9          Hansen, N. Long-Term Memory Dysfunction in Limbic Encephalitis. Frontiers in Neurology 10 (2019). https://doi.org/10.3389/fneur.2019.00330

10        Titulaer, M. J. et al. Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol 12, 157-165 (2013). https://doi.org/10.1016/s1474-4422(12)70310-1

11        Gibson, L. L., McKeever, A., Coutinho, E., Finke, C. & Pollak, T. A. Cognitive impact of neuronal antibodies: encephalitis and beyond. Translational Psychiatry 10 (2020). https://doi.org/10.1038/s41398-020-00989-x

12        Kelley, B. P. et al. Autoimmune Encephalitis: Pathophysiology and Imaging Review of an Overlooked Diagnosis. American Journal of Neuroradiology 38, 1070-1078 (2017). https://doi.org/10.3174/ajnr.a5086

13        CORSELLIS, J. A. N., GOLDBERG, G. J. & NORTON, A. R. “LIMBIC ENCEPHALITIS” AND ITS ASSOCIATION WITH CARCINOMA. Brain 91, 481-496 (1968). https://doi.org/10.1093/brain/91.3.481

14        Finke, C. et al. Structural Hippocampal Damage Following Anti-N-Methyl-D-Aspartate Receptor Encephalitis. Biological Psychiatry 79, 727-734 (2016). https://doi.org/10.1016/j.biopsych.2015.02.024

15        Haselmann, H. et al. Human Autoantibodies against the AMPA Receptor Subunit GluA2 Induce Receptor Reorganization and Memory Dysfunction. Neuron 100, 91-105.e109 (2018). https://doi.org/10.1016/j.neuron.2018.07.048

16        Planagumà, J. et al. Ephrin‐B2 prevents N‐methyl‐D‐aspartate receptor antibody effects on memory and neuroplasticity. Annals of Neurology 80, 388-400 (2016). https://doi.org/10.1002/ana.24721

17        Hruska, M. & Dalva, M. B. Ephrin regulation of synapse formation, function and plasticity. Molecular and Cellular Neuroscience 50, 35-44 (2012). https://doi.org/10.1016/j.mcn.2012.03.004

Figure 1 and Table 1 made by Ryan Rahman in BioRender.com.

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On June 16 th, 2022, Tabitha Orth, President and Founder of International Autoimmune Encephalitis Society officially became the 7,315 th “point of light”. Recognized for the volunteer work she and IAES has done to spark change and improve the world for those touched by Autoimmune Encephalitis. The award was founded by President George H.W. Bush in 1990.

 

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Become an Advocate by sharing your story. It may result in accurate diagnosis for someone suffering right now who is yet to be correctly identified. Submit your story with two photos to IAES@autoimmune-encephalitis.org  

 

 

International Autoimmune Encephalitis Society (IAES), home of the AEWarrior®, is the only Family/Patient-centered organization that assists members from getting a diagnosis through to recovery and the many challenges experienced in their journey. Your donations are greatly appreciated and are the direct result of IAES’ ability to develop the first product in the world to address the needs of patients, Autoimmune Encephalitis Trivia Playing Cards. Every dollar raised allows us to raise awareness and personally help Patients, Families, and Caregivers through their Journey with AE to ensure that the best outcomes can be reached. Your contribution to our mission will help save lives and improve the quality of life for those impacted by AE.   Trivia Playing cards 3 FB 500x419 - Memory and Autoimmune Encephalitis For this interested in face masks, clothing, mugs, and other merchandise, check out our AE Warrior Store!  This online shop was born out of the desire for the AE patient to express their personal pride in fighting such a traumatic disease and the natural desire to spread awareness. Join our AE family and help us continue our mission to support patients, families and caregivers while they walk this difficult journey.   AE Warrior Store 300x200 - Memory and Autoimmune Encephalitis

Be a part of the solution by supporting IAES with a donation today.

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What is the connection between cancer and autoimmune encephalitis?

What is the connection between cancer and autoimmune encephalitis?

November 29, 2023 | by Sophie Liebergall and Ayan Mandal, PennNeuroKnow and IAES Collaboration

A message from IAES Blog Staff:

The staff at IAES is proud to present to all of you another wonderful article/blog from the amazing team at PennNeuroKnow. Since 2019 IAES has been extremely lucky to be in partnership with the PennNeuroKnow(PNK) team to help us all better understand complex medical issues related to AE and neurology in general. The talented PNK team continues to keep us up-to-date and help clarify the complexities we face each day along our AE journey, and we are eternally grateful! You can find out much more about this stellar group at: https://pennneuroknow.com/

—-

Introduction

When a patient is admitted to the hospital with symptoms that suggest a diagnosis of autoimmune encephalitis (AE), doctors start ordering a dizzying array of lab tests and scans. Although AE is a disease of the brain, many of these tests, such as CT scans of the chest or ultrasounds of the pelvis, don’t seem to have much to do with the brain at all. The purpose of these scans is to search for a tumor that lies somewhere in the body. The reason why doctors conduct this search for a tumor is because some AE patients have a subtype of the disease, called paraneoplastic encephalitis, in which their disease is actually caused by a tumor outside of the brain. In this post we will shed some light on paraneoplastic encephalitis, why it occurs, and how its treatment compares to other types of AE.

What is paraneoplastic encephalitis?

As we explained in a previous post, paraneoplastic encephalitis is a type of AE caused by a tumor somewhere outside of the brain. The symptoms of paraneoplastic encephalitis, which could include seizures, memory loss, confusion, and dizziness, are often the first signs of an underlying cancer.1 For this reason, a patient who is suspected to have autoimmune encephalitis will often undergo scans of each organ in their body (colloquially called a “pan-scan”) to search for a possible cancer that may be responsible for the patient’s symptoms.

Some malignancies that are especially likely to trigger paraneoplastic encephalitis include cancers of the breast, ovaries, and lungs.2 But why would a tumor in one of these organs outside the brain cause the immune system to attack the brain? To understand why, we need to learn a bit about how the immune system responds to cancer.

How does the immune system respond to cancer?

Though it may be an unsettling thought, abnormal cells with the potential to become cancer are born in the body all the time. We tend not to be aware of this because most of the time the immune system successfully squashes these abnormal cells before they become a full-blown cancer. Many scientific experiments have proven how effectively the immune system monitors the body for these cancer cells. For example, when mice are genetically engineered to lack key immune cells, they become much more susceptible to developing tumors – implying that the removed immune cells were necessary to prevent tumor development.3 Because the immune system plays a crucial role in protecting the body from cancer, many cutting edge cancer treatments work by empowering the patient’s own immune system to kill their cancer cells.

The immune system prevents the growth of tumors by reacting to abnormal proteins that are a sign of cancer. Tumors tend to produce mutated proteins that are not found in the healthy body. Once an immune cell sniffs out one of these proteins it hasn’t seen before, it eats the protein and starts sending out alarm bells to other immune cells. These alarm signals tell one set of immune cells, called B cells, to start making antibodies that bind to this suspicious protein. Antibodies function like little flags that mark the cell with the mutated protein for destruction. Specifically, in the case of paraneoplastic AE, the initial alarm bells also activate another set of immune cells called cytotoxic T cells.4,5 The role of cytotoxic T cells is to expertly survey for cells that have been marked as harmful as potentially cancerous. Then, once they find these potentially dangerous cells, they release toxins that kill the cells (Figure 1).

immune system cancer - What is the connection between cancer and autoimmune encephalitis?

Figure 1. How the immune system responds to cancer. 1. A “first-line” immune cell chews up breast tumor cells, which contain proteins not normally found in breast cells. These proteins are represented as crabs. 2. The “first-line” immune cell realizes that it has eaten a cancer cell and so it sends signals that activate B and cytotoxic T cells. 3. Activated B cells produce antibodies which bind to the crab proteins. At the same time, activated cytotoxic T cells start to look for the cells that are tagged by the antibodies. 4. Antibodies bind to the crab protein in the breast tumor cells. Once the cytotoxic T cells find these tagged cells, they release toxins to kill the breast tumor cells. This figure was created using Biorender.com.

 

Why do some people get paraneoplastic encephalitis?

Sometimes, tumors produce suspicious proteins that look very similar to proteins also found in the brain. For example, some breast cancers can produce a protein that looks very similar to a protein inside of specific neurons in the cerebellum (a part of the brain important for balance and coordination).6 In this way, as the immune system prepares for battle against the breast cancer, sometimes the brain with it’s cancer look-alike cells can get caught in the crossfire. When an immune cell detects the breast cancer cells, it will chew up the proteins in those breast cancer cells, including the ones that look like cerebellum proteins. Because these cerebellum proteins were found inside a breast cancer cell, the immune cell thinks that they are harmful. Therefore, the immune cell will tell B cells to make antibodies targeting the cerebellum protein. At the same it will also tell cytotoxic T cells to kill all cells with the cerebellum protein. When these cytotoxic T cells try to find and kill more tumor cells, they may also try to kill healthy cells in the cerebellum that  make the protein.7

immune system paraneoplastic - What is the connection between cancer and autoimmune encephalitis?

Figure 2. How the immune system responds to cancer causes paraneoplastic AE. 1. A “first-line” immune cell chews up breast tumor cells, which contain proteins not normally found in breast cells. These proteins are represented as crabs. 2. The “first-line” immune cell realizes that it has eaten a cancer cell and so it sends signals that activate B and cytotoxic T cells. 3. Activated B cells produce antibodies which bind to the crab proteins. At the same time, activated cytotoxic T cells start to look for the cells that are tagged by the antibodies. 4. Because the crab protein is normally found in healthy cerebellum cells, antibodies bind to the crab protein in the cerebellum. Once the cytotoxic T cells find tagged cerebellum cells, they release toxins to kill the cerebellum cells.

What is the difference between paraneoplastic and non-paraneoplastic AE?

In the case of paraneoplastic encephalitis, the immune system is trying to do its job correctly by killing tumor cells, and the harm that it does to healthy neurons is collateral damage.7 This is different than cases of non-paraneoplastic encephalitis, where the problem lies within the immune system itself. In non-paraneoplastic AE, the immune system mistakenly decides that proteins that are normally found on the outside of neurons are actually harmful.7 (See this previous IAES post for a more detailed explanation of antibodies against proteins on the inside vs. the outside of cells.) In both paraneoplastic and non-paraneoplastic autoimmune encephalitis, the patient’s immune system tells B cells to make antibodies that target a neuronal protein. These antibodies then bind to the target protein in neurons and cause the patient to experience symptoms. However, cases of paraneoplastic encephalitis tend to involve more permanent damage to the neurons and more severe and long-lasting symptoms than cases of non-paraneoplastic autoimmune encephalitis. This is because the tumor also activates cytotoxic T cells in addition to B cells. These cytotoxic T cells are responsible for the increased damage and more severe symptoms in paraneoplastic AE.9

 

Paraneoplastic Encephalitis

Non-paraneoplastic Autoimmune Encephalitis

Target Protein

Usually intracellular proteins (e.g. Hu, Ma1/2, Ri), sometimes cell surface proteins

Cell surface proteins (e.g. NMDA receptor, GABABreceptor, Caspr2)

Age

Mostly older people

All ages

Tumor present

Yes

No

Immune system involvement

Cytotoxic T cells + antibodies

Antibodies

Response to treatment

Treatment less effective

Generally good response to treatment

Adapted from Rosenfeld et al. Neurol Clin Pract. 20128

How is paraneoplastic autoimmune encephalitis treated?

When treating paraneoplastic AE, doctors often use the same therapies that are used for non-paraneoplastic AE.10The majority of these treatments, such as plasma exchange, IVIg, and rituximab, are aimed at eliminating the antibodies that target the neuronal protein.10-12 (You can learn more about antibody-targeting treatments in this post.) For patients with non-paraneoplastic AE, once the antibodies are no longer bound to the neuronal proteins their symptoms often go away. But, unfortunately, in the case of paraneoplastic encephalitis, both antibody-producing B cells and cytotoxic T cells are activated.9 The cytotoxic T cells can unfortunately do more permanent damage to their neurons than the antibodies alone. Because of this, patients with paraneoplastic encephalitis tend to have poorer responses to treatment when compared to patients with non-paraneoplastic autoimmune encephalitis.13

When treating paraneoplastic encephalitis, it is very important to treat the underlying cause of the encephalitis: the cancer.13-14 When patients receive treatment for their cancer, either in the form of surgery to remove the cancer or chemotherapy drugs to shrink the cancer, they can sometimes see some improvement in their paraneoplastic encephalitis symptoms.13 When treating patients with paraneoplastic AE, doctors are often faced with a particular challenge: the immune system serves as both friend and foe. On one hand, the immune system is what is causing the patient’s paraneoplastic AE symptoms. While on the other hand, as discussed above, a strong immune system is important for keeping cancer at bay. As such, doctors often must carefully consider whether they want to give patients drugs that suppress the immune system, especially if the patient is actively undergoing treatment for their cancer.9

There are already a number of new therapies on the horizon for paraneoplastic AE that will hopefully improve the symptoms and long-term outcomes of this disorder. For example, understanding the role of cytotoxic T cells in paraneoplastic AE has led scientists to start to test treatments that directly target cytotoxic T cells.15 Conducting clinical trials in a relatively rare disorder like paraneoplastic AE can be especially challenging. But a growing awareness among physicians about paraneoplastic AE has led to an increased number of patients receiving a proper diagnosis for their neurologic symptoms. Clinical trials that enroll larger numbers of patients with paraneoplastic AE will hopefully hasten the development of more effective treatments.

References:

  1. Overview of paraneoplastic syndromes of the nervous system – UpToDate. https://www.uptodate.com/contents/overview-of-paraneoplastic-syndromes-of-the-nervous-system.
  2. Dalmau, J. & Rosenfeld, M. R. Paraneoplastic syndromes of the CNS. Lancet Neurol 7, 327–340 (2008).
  3. Shankaran, V. et al. IFNgamma and lymphocytes prevent primary tumour development and shape tumour immunogenicity. Nature 410, 1107–1111 (2001).
  4. Raskov, H., Orhan, A., Christensen, J. P. & Gögenur, I. Cytotoxic CD8+ T cells in cancer and cancer immunotherapy. Br J Cancer 124, 359–367 (2021).
  5. Cano, R. L. E. & Lopera, H. D. E. Introduction to T and B lymphocytes. in Autoimmunity: From Bench to Bedside [Internet] (El Rosario University Press, 2013).
  6. Paraneoplastic cerebellar degeneration – UpToDate. https://www.uptodate.com/contents/paraneoplastic-cerebellar-degeneration.
  7. Melzer, N., Meuth, S. G. & Wiendl, H. Paraneoplastic and non-paraneoplastic autoimmunity to neurons in the central nervous system. J Neurol 260, 1215–1233 (2013).
  8. Neumann, Harald, Isabelle M. Medana, Jan Bauer, and Hans Lassmann. “Cytotoxic T Lymphocytes in Autoimmune and Degenerative CNS Diseases.” Trends in Neurosciences 25, no. 6 (June 1, 2002): 313–19.https://doi.org/10.1016/S0166-2236(02)02154-9.
  9. Chaigne, Benjamin, and Luc Mouthon. “Mechanisms of Action of Intravenous Immunoglobulin.” Transfusion and Apheresis Science 56, no. 1 (February 1, 2017): 45–49. https://doi.org/10.1016/j.transci.2016.12.017.
  10. Lehmann, Helmar C., Hans-Peter Hartung, Gerd R. Hetzel, Olaf Stüve, and Bernd C. Kieseier. “Plasma Exchange in Neuroimmunological Disorders: Part 1: Rationale and Treatment of Inflammatory Central Nervous System Disorders.” Archives of Neurology 63, no. 7 (July 1, 2006): 930–35.https://doi.org/10.1001/archneur.63.7.930.
  11. Taylor, Ronald P., and Margaret A. Lindorfer. “Drug Insight: The Mechanism of Action of Rituximab in Autoimmune Disease—the Immune Complex Decoy Hypothesis.” Nature Clinical Practice Rheumatology 3, no. 2 (February 2007): 86–95. https://doi.org/10.1038/ncprheum0424.
  12. Dalmau, Josep, and Myrna R. Rosenfeld. “Update on Paraneoplastic Neurologic Disorders.” Community Oncology 7, no. 5 (May 1, 2010): 219–24.
  13. Gultekin, S. H. et al. Paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients. Brain 123 ( Pt 7), 1481–1494 (2000).
  14. Bastiaansen, Anna E M, Adriaan H C de Jongste, Marienke A A M de Bruijn, Yvette S Crijnen, Marco W J Schreurs, Marcel M Verbeek, Daphne W Dumoulin, Walter Taal, Maarten J Titulaer, and Peter A E Sillevis Smitt. “Phase II Trial of Natalizumab for the Treatment of Anti-Hu Associated Paraneoplastic Neurological Syndromes.” Neuro-Oncology Advances 3, no. 1 (January 1, 2021): vdab145.https://doi.org/10.1093/noajnl/vdab145.

Figures 1 and 2 were created using Biorender.com.

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Tabitha Orth 300x218 - What is the connection between cancer and autoimmune encephalitis?

 

 

On June 16 th, 2022, Tabitha Orth, President and Founder of International Autoimmune Encephalitis Society officially became the 7,315 th “point of light”. Recognized for the volunteer work she and IAES has done to spark change and improve the world for those touched by Autoimmune Encephalitis. The award was founded by President George H.W. Bush in 1990.

 

guidestar platinum logo 300x300 1 e1605914935941 - What is the connection between cancer and autoimmune encephalitis?

 

Become an Advocate by sharing your story. It may result in accurate diagnosis for someone suffering right now who is yet to be correctly identified. Submit your story with two photos to IAES@autoimmune-encephalitis.org  

 

 

International Autoimmune Encephalitis Society (IAES), home of the AEWarrior®, is the only Family/Patient-centered organization that assists members from getting a diagnosis through to recovery and the many challenges experienced in their journey. Your donations are greatly appreciated and are the direct result of IAES’ ability to develop the first product in the world to address the needs of patients, Autoimmune Encephalitis Trivia Playing Cards. Every dollar raised allows us to raise awareness and personally help Patients, Families, and Caregivers through their Journey with AE to ensure that the best outcomes can be reached. Your contribution to our mission will help save lives and improve the quality of life for those impacted by AE.   Trivia Playing cards 3 FB 500x419 - What is the connection between cancer and autoimmune encephalitis? For this interested in face masks, clothing, mugs, and other merchandise, check out our AE Warrior Store!  This online shop was born out of the desire for the AE patient to express their personal pride in fighting such a traumatic disease and the natural desire to spread awareness. Join our AE family and help us continue our mission to support patients, families and caregivers while they walk this difficult journey.   AE Warrior Store 300x200 - What is the connection between cancer and autoimmune encephalitis?

Be a part of the solution by supporting IAES with a donation today.

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Our website is not a substitute for independent professional medical advice. Nothing contained on our website is intended to be used as medical advice. No content is intended to be used to diagnose, treat, cure or prevent any disease, nor should it be used for therapeutic purposes or as a substitute for your own health professional's advice. Although THE INTERNATIONAL AUTOIMMUNE ENCEPHALITIS SOCIETY  provides a great deal of information about AUTOIMMUNE ENCEPHALITIS, all content is provided for informational purposes only. The International Autoimmune Encephalitis Society  cannot provide medical advice.


International Autoimmune Encephalitis Society is a charitable non-profit 501(c)(3) organization founded in 2016 by Tabitha Andrews Orth, Gene Desotell and Anji Hogan-Fesler. Tax ID# 81-3752344. Donations raised directly supports research, patients, families and caregivers impacted by autoimmune encephalitis and to educating healthcare communities around the world. Financial statement will be made available upon request.

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