Autism and Palilalia
In this video, we will discuss some common autistic behaviours such as Echolalia, Palilalia, Scripting, and Vocal Stimming.
“Autism and palilalia – why is palilalia considered a sign of autism?”
“Ten Early Signs of Autism (UPDATED)”
10 Early Signs of Autism (UPDATED)
How can you tell if your child is autistic? This video is designed to provide you with answers and includes clinical examples of various autistic individuals. We mention echolalia as an example of speech, but it’s worth noting that in this particular case, Alistair was also displaying palilalia, which involves constant repetition.
New nanoparticles have been discovered to be effective for treating rheumatoid arthritis.
CREDIT Institute for Basic Science
A team of scientists led by Koo Sagang from Seoul National University and the Center for Nanoparticle Research within the Institute for Basic Science (IBS), in collaboration with researchers from the Korea Institute of Science and Technology (KIST) and Seoul National University, has developed a new solution for the treatment of rheumatoid arthritis (RA).
Rheumatoid arthritis (RA) is a chronic disease that, unfortunately, has no cure. The disease triggers a mix of troublesome symptoms such as inflamed joints, harmful cytokines, and immune system imbalances, which work together to create a relentless cycle of worsening symptoms. While targeting some of these factors can provide short-term relief, others remain unresolved, leading to a frustrating cycle of remission and flare-ups.
“An important challenge in treating rheumatoid arthritis (RA) is the difficulty in returning the immune system to a healthy state. This results in the body being unable to regulate the ongoing production of harmful substances such as reactive oxygen species (ROS) and inflammatory cytokines, which leads to persistent inflammation and discomfort.”
In essence, the ideal treatment for rheumatoid arthritis (RA) should offer immediate relief from inflammation and symptoms and target the underlying cause by restoring the immune system to its normal, balanced state.
New nanoparticle-based system as a solution
The new platform involves immobilizing ceria nanoparticles (Ce NPs) onto mesenchymal stem cell-derived nanovesicles (MSCNVs). These components can hinder different pathogenic factors, allowing them to work individually and cooperatively to achieve a comprehensive treatment.
Ce nanoparticles can scavenge the overproduced reactive oxygen species (ROS) in rheumatoid arthritis (RA)-affected knee joints. They also induce polarization of M1 macrophages into M2, leading to immediate relief of inflammation and symptoms.
MSCNVs – deliver immunomodulatory cytokines, which turn dendritic cells (DC) into tolerogenic dendritic cells (tDCs). This consequently generates regulatory T cells for long-term immune tolerance.
In short, this approach aims to bridge both innate and adaptive immunity to achieve both short-term pain relief as well as convert the tissue environment into an immune-tolerant state to prevent the recurrence of symptoms.
Researchers confirmed the efficacy of this approach using a collagen-induced arthritis mouse model. The Ce-MSCNV system was able to comprehensively treat and prevent RA by simultaneously relieving the immediate and restoring T cell immunity. Supporting data suggest that improvement in conditions can be achieved after only a single-dose treatment.
The mice treated with the Ce-MSCNV combination fared far better than those treated using the Ce NP or MSCNV group. This demonstrates the synergy between anti-inflammation and immunomodulation and underlines the importance of the combined therapy for effective RA treatment. In addition, Ce-MSCNV administration before booster injection markedly reduced the incidence and severity of symptoms, supporting the prophylactic potential of these nanoparticles.
First author KOO Sagang stated, “One of the hardest decisions in intractable disease therapy is determining how long the treatment should take. For RA, it would not be appropriate to stop treatment just because the target marker is stabilized. A safer indicator should be that the innate and adaptive components of the collapsed immune system are normalized to protect the body.”
Koo believes that the strategy adopted by Ce-MSCNVs, where different treatment mechanisms work together, provides a unique advantage. Furthermore, she predicts that a similar approach would also apply to other intractable, inflammatory, and autoimmune diseases for this purpose. The components within the system may also be modified. For example, other catalysts for generating ROS or other cell-derived nanovesicles could be utilized depending on the types of diseases. Overall, this study proves the potential of a hybrid nanoparticle system for the comprehensive treatment of autoimmune disease and modulation of the immune system.
Dr Sarah Morrow and cognitive impairment in MS patients
“A model that helps to explain why some patients with multiple sclerosis experience seizures.”
This is an image from the research is featured on the cover of volume 346 (pages 409-422) of the journal <i>Neuroscience</i>. CREDIT Elsevier.
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system that affects nearly 2.3 million people worldwide. MS is triggered when the immune system attacks the protective covering around nerve fibers, called the myelin sheath. The resulting “demyelination” damages nerve cells and impairs the exchange of information between the brain and body and within the brain itself.
When the protective covering around nerve fibers wears off, nerve signals can slow down or stop. Depending on where the damage occurs, this can lead to impaired vision, sensation, and use of limbs. If the disease destroys nerve fibers, it can lead to permanent paralysis.
“In addition to this, individuals with multiple sclerosis (MS) are three to six times more likely to develop seizures—abnormal hyperactivity of nerve cells—compared to the rest of the population. Despite this increased occurrence, little research has been conducted to explore the reasons behind these seizures in MS patients.”
In a mouse model, a team of scientists at the University of California, Riverside, has discovered that chronic demyelination is closely linked to, and likely the cause of, seizures. The researchers reported their findings in the journal Neuroscience. They also observed that specific neurons in the brain, known as “parvalbumin interneurons,” which are crucial for controlling hyperactivity, undergo changes and are lost when extensive demyelination occurs in the brain’s cortex and hippocampus.
“Demyelination causes damage to axons and neuronal loss. Specifically, parvalbumin interneurons are lost in mice, resulting in a shift from reduced activity to increased activity, which could be a cause of seizures,” explained Seema Tiwari-Woodruff, an associate professor of biomedical sciences in the UC Riverside School of Medicine, whose laboratory conducted the research. “It’s highly likely that this is also happening in MS patients who experience seizures.”
Tiwari-Woodruff and her team induced demyelination in mice in the lab by feeding them a diet containing cuprizone, a copper-binding substance that causes damage to oligodendrocytes, the brain cells that produce myelin. After nine weeks of being fed cuprizone, the majority of the mice started having seizures.
“Without myelin, axons are vulnerable,” said Tiwari-Woodruff. “They develop blebs – ball-like structures that hinder the transport of important proteins and conduction of electrical signals. In some instances, significant axon damage can lead to neuronal loss. In both MS and our mouse model, parvalbumin interneurons are more vulnerable and likely to die. This causes the inhibition to be removed and induce seizures. Thus, axonal and neuronal survival may be directly tied to the trophic support provided by myelin.”
In another study, after nine or twelve weeks, the researchers stopped feeding the mice the cuprizone diet. Oligodendrocytes began to repopulate the demyelinated areas and remyelinate the intact but myelin-stripped axons. Future studies will assess seizure activity with remyelination.
“Does remyelination affect seizure activity? Can we accelerate remyelination with drugs to provide relief for MS patients? We are interested in addressing these questions,” Tiwari-Woodruff said.
Her team recently received a pilot grant from the National Multiple Sclerosis Society. They will be comparing postmortem brain tissue from MS patients with seizures to those without in order to understand the cellular basis of seizures in MS. Additionally, they will use their findings to assess how accurately the cuprizone mouse model replicates the changes observed in humans.
“We want to know if the tissues exhibit the same characteristics as those in our mouse model,” said Tiwari-Woodruff. “Our initial findings in postmortem tissue indicate significant similarities between the two. We now have a mouse model that we can utilize to test and propose potential therapeutic treatments. Once developed, these drugs, designed to reduce hyperactivity and decrease the occurrence of seizures, could also benefit patients with epilepsy.”