LGI1 Antibodies

Leucine-rich glioma-inactivated protein 1 (LGI1)

Regulates voltage-gated potassium channels assembled from KCNA1, KCNA4 and KCNAB1. It slows down channel inactivation by precluding channel closure mediated by the KCNAB1 subunit.

Ligand for ADAM22 that positively modulates synaptic transmission mediated by AMPA-type glutamate receptors (By similarity). Plays a role in curbing the creation of MMP1/3 throughout the phosphatidylinositol 3-kinase/ERK pathway.

Gene Information

Human
Gene Name:	LGI1
Uniprot:	O95970
Entrez:	9211

Family

Belongs to:
No superfamily

Alternative Names

ADLTE; ADPAEF; ADPEAF; BB130740; epilepsy, partial; Epitempin; Epitempin-1; EPT; EPTleucine-rich glioma-inactivated protein 1; ETL1; ETL1epitempin-1; IB1099; leucine-rich, glioma inactivated 1; LGI1

Molecular Weight

Mass (kDA):
63.818 kDA

Genomic Context

Human
Location:	10q23.33
Sequence:	10; NC_000010.11 (93757809..93798174)

Tissue Specificity

Predominantly expressed in neural tissues, especially in brain. Expression is reduced in low-grade brain tumors and significantly reduced or absent in malignant gliomas. Isoform 1 is absent in the cerebellum and is detectable in the occipital cortex and hippocampus; higher amounts are observed in the parietal and frontal cortices, putamen, and, particularly, in the temporal neocortex, where it is 3.5 times more abundant than in the hippocampus (at protein level). Isoform 3 shows the highest expression in the occipital cortex and the lowest in the hippocampus (at protein level).

Subcellular Localizations

Secreted. Cell junction, synapse. Isoform 1 but not isoform 2 is secreted. Isoform 1 is enriched in the Golgi apparatus while isoform 2 accumulates in the endoplasmic reticulum.

Diseases

• Epilepsy
• Epilepsy, Temporal Lobe
• Epilepsies, Partial
• Glioma
• Encephalitis
• Lateral Temporal Epilepsy
• Neoplasms
• Limbic Encephalitis
• Partial Seizure
• Malignant Neoplasms
• Malignant Paraganglionic Neoplasm
• Febrile Convulsions

• Autoimmune Reaction
• Nervousness
• Aphasia
• Nervous System Disorder
• Encephalopathies
• Autoimmune Diseases

Pathways

• Pathogenesis
• Secretion
• Synaptic Transmission
• Localization
• Brain Development
• Protein Secretion
• Myelination
• Axon Guidance
• Glycosylation
• Methylation
• Cell Death
• Protein Folding
• Cell Growth

• Cellular Homeostasis
• Immune Response
• Neurogenesis
• Cell Maturation
• Sensitization
• Swimming
• System Development

PTMs

• Glycosylation
• Phosphorylation

• Palmitoylation
• Methylation

Research Areas

• Neuroscience

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/LGI1

Best Uses Of The LGI1 Marker

The LGI1 marker has been associated with the diagnosis of glioma, however, it is believed to play an important role in other cancers too. It is part of a set of related proteins that contains leucine-rich repeatsthat act as transmembrane signals molecules. LGI1 is a ligand of the ADAM22 metalloprotease. Autodominant temporal and lateral epilepsy is caused by mutations in LGI1. This form of focal seizures has an auditory component that is the predominant.

Memory loss

Recent studies have indicated that LGI1 markers may be related to memory deterioration. Majoie and colleagues8 found that 89 percent of patients with a course of 8-months of disease showed some memory impairment. Three cases showed a combination disorientation/memory disorder. These findings raise questions about LGI1 LE's cause and treatment options.

The LGI1 gene is expressed in the CA3 subfield of the hippocampal hippocampal. It is involved in pattern completion, pattern separation and encoding. LGI1 is essential to memory processing. It is essential to retrieve the entire memory from a partial clue. LGI1 proteins are essential to the formation of distinct memory representations that are not overlapping. In this study, participants were asked to differentiate specific words from very similar lure and distraction items. Patients with significantly higher levels of LGI1 proteins on the brain MRI were more difficult in identifying words that were targeted.

Anti-LGI1 encephalitis on the other hand is associated with diminished memory, decreased hippocampal volumes and decreased hippocampal microstructural integrity. Higher levels of structural damage to the hippocampal were associated with more severe clinical outcomes. Furthermore, patients with the disease had poorer memory performance when treatment was delayed. In addition, a longer course of FBDS was associated with a decrease in pallidum volume, another indication of memory deterioration after anti-LGI1 encephalitis.

Sleep disorders

The LGI1 gene is a genetic marker that increases the risk of sleep disorders in various forms. The link between sleep disorders and LGI1 is best demonstrated through longitudinal studies of patients with rapid eye movement sleep disorder (REM-SBD). Two associations have been identified with REM-SBD by researchers: Elliott JE and Tribl GG. The two other ones have demonstrated links with narcoleptic patients as well as secondary REM-SBD.

This marker can be used as a biomarker for identifying certain neurodegenerative diseases. The LGI1 gene is most helpful in sleep disorders related to Lewy body syndrome, which is a form Parkinson's disease. Other sleep disorders can be identified by using this marker. There are many ways to use this gene to identify patients with REM-SBD. However, the LGI1 gene is most effective in sleep disorders that cause REM-SBD.

One study looked at an average of 203 consecutive RBD patients. Most common symptoms were violent thrashing and slipping out of the bed. Patients also reported vocalizations. The movements could range from mild hand gestures to more violent and intimidating that include punching and kicking. You could hurt yourself, strike a partner, or be thrown out of bed in the course of sleep. The most risk is self-injury.

The LGI1 gene was discovered in the cerebellum, serum, and the brain. The gene is expressed extensively within the CA3 subfield. It is involved in memory processing and pattern completion. It is a major gene in the LGI1 region that is responsible for the ability of a person to learn new information. It has been suggested that LGI1 gene expression might be directly related to verbal memory performance.

Epilepsy

The LGI1 antibody is present in the cerebrospinal liquid of patients suffering from leucine-rich glioma type encephalitis (LRGE). It is linked to neuronal damage in the brain that can cause memory and behavior disorders. LGI1 antibodies are linked to more severe cases. This may be due to the increase in antibodies to LGI1.

LGI1-antibody encephalitis is defined by a mix of sensory and motor events. These include body shuddering, automatisms, and partial seizures. Additionally, a higher seizures are associated with less functional recovery after two years. Patients with high seizure frequency should seek out proactive treatment to lessen the effects of these seizures.

The LGI1 marker has a number of advantages. It can aid in predicting effectiveness of immunotherapy for epilepsy patients. It has also been proven that it can improve the prognosis of patients with repeated seizures. It can improve the prognosis of epilepsy patients over time. Patients who have recurrent epileptic seizures can assess the antibody level of LGI1.

LGI1 antibody is a protein that is secreted by the brain, is associated with auto-immune and genetic seizures. In autosomal dominant epilepsy, which has auditory features mutations in LGI1 cause the onset of seizures. In patients suffering from LGI1 antibodies, autoantibodies against LGI1 result in neurodegeneration and limbic encephalitis.

CJD

The patient was diagnosed with progressive dementia, psychiatric symptoms , and hyponatremia. The EEG of the patient revealed no PSWCs and was in direct opposition to the clinical diagnosis. His family members refused to perform an autopsy due to the fact that he later was diagnosed with acute pancreatitis. CJD was later diagnosed in the patient.

The most common sign of CJD is dementia, which is defined by rapid onset of symptoms and twitching of the hands and face. An MRI scan of his brain showed abnormalities in his basal ganglia. The man's diagnosis of CrJ disease was confirmed by another academic medical center. FBD seizures could be a sign of nonparaneoplastic anti-LGI1 syndrome. His symptoms completely disappeared after treatment.

The LGI1-antibody test for CJD is a precise tool for diagnosing the disease. Antibodies against LGI1 are highly specific and are able to distinguish the symptoms of CJD from other conditions. CJD can be caused by antibodies. The LGI1-antibody in some patients might not be specifically for CJD and could be a sign of another condition.

Anti-LGI1 antibody Encephalitis

The diagnosis of encephalitis triggered by anti-LGI1 antibody was made at Xuanwu Hospital, Capital Medical University, when the patient met the criteria. Anti-LGI1 antibody was found in cerebrospinal fluid (CSF) as well as serum samples. The patient's condition was tracked for two years, and during that time the majority of patients showed improvement in cognitive function and memory.

Anti-LGI1 antibody encephalitis can cause progressive memory loss, confusion and sleep disruption. Low sodium levels and seizures are often caused by this disorder. In addition , patients suffering from anti-LGI1 encephalitis might have behavioral changes and possibly comorbid tumors. If any of these symptoms are present, patients must seek immediate medical attention. Although there isn't a cure, immunotherapy can be used to decrease seizure activity.

The most commonly reported symptoms of anti-LGI1 the encephalitis include clonic, tonic and partial seizures. About 20%-40%11 of patients suffering from anti-LGI1-related encephalitis will also experience FBDS. These are brief unconscious seizures that affect the face or arm. They are typically accompanied by dystonia. The symptoms of anti-LGI1 antibody encephalitis can be severe, mild and sometimes fatal.

Inter-ictal EEG in patients suffering from anti-LGI1 encephalitis shows sharp-waves at the sphenoid electrodes. It is possible to combine of immunosuppressive therapy and plasma exchange. Certain patients experience relapses after receiving treatment, but these methods can improve cognition. If diagnosed early, anti-LGI1 is treatable.

Hyponatremia

Hyponatremia can be triggered by strenuous physical exertion such as running marathons. It can be caused by excessive intake of water, but other factors such as body mass, hormonal changes in exercise, and body mass could also play a part in. This article will focus on the causes and treatment of hyponatremia. Check out the article below to discover more about this condition.

Hyponatremia is one of the most serious diseases. A lot of these diseases cause inflammation. Hyponatremia is a possible result of the disease. Inflammation is a cause of many diseases, such as acute respiratory distress syndrome, bacterial infections, and tuberculosis. Other diseases that are a result of inflammation include tuberculosis, pneumonia meningitis, encephalitis and pneumonia. Alongside these classic instances, hyponatremia also has been associated with dengue and malaria infections, as well as other diseases.

Your doctor is likely to be able and able to determine you for hyponatremia. You could be experiencing one or more of these symptoms: more frequent urination and vomiting, as well as depletion of the volume. You should immediately contact your doctor if you experience any of the symptoms. Most people will recover quickly when they receive the correct treatment. Below are the symptoms and treatments for hyponatremia.

A recent study found a link between mild hyponatremia as well as injurious falls in elderly medical patients. The results of this study are not generalizable as they were conducted in a MUPA unit and a ED. MUPA patients however, are more likely to sustain injuries related to falls. A study of the relationship between mild hyponatremia, falls, and the MUPA patient population could be useful.