Pancreatic cancer is closely linked to the nervous system, according to researchers from the German Cancer Research Center (DKFZ) and the Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM). Their recent study, published in Nature, reveals that pancreatic tumors actively reprogram neurons to support their growth.
Featuring:
Paola Arlotta.
Golub Family Professor of Stem Cell and Regenerative Biology, Harvard University.
Chair, harvard department of stem cell and regenerative biology.
Associate member, stanley center for psychiatric research, broad institute.
This episode is all about brain organoids. Cerebral organoids or brain organoids were developed in 2013 by Madeline Lancaster and Jürgen Knoblich. Brain organoids are also called mini-brains and they are a powerful tool to grow brain-like structures in petri dishes. Brain organoids enable studies on the development of brains, brain diseases or brain infections. In this video, we will talk how we can make brain organoids and how we use brain organoids.
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0:00 — Introduction to Brain Organoids.
1:29 — What are Brain Organoids?
2:41 — How to Make Brain Organoids.
5:09 — Studying Development with Brain Organoids.
6:49 — Zika Virus, COVID-19 and Brain Organoids.
8:44 — Schizophrenia, Autism, Depression and Brain Organoids.
Okay, so what are brain organoids? Brain organoids or cerebral organoids are laboratory-grown structures which mimic parts of the brain. Brain organoids establish regions with multiple layers of neurons comparable to the developing brain. However, cells within brain organoids are less specific compared to cells we find in the brain. We also do not find any specific \.
Can kung fu fighting change what’s inside your cranium? Even brief periods of martial-arts training can produce benefits in brain activity and bodily health.
Huntington’s disease is a neurodegenerative disorder that is usually fatal about 15 to 20 years after a patient is diagnosed. It is known to be caused by an aberrant repetitive sequence (CAG) in the huntingtin gene. Unaffected people carry fewer than 35 of these CAG repeats, while Huntington’s patients have more than 40 CAG repeats, which get longer, or expand over their lifetime. Scientists have now revealed that a specific subset of genes related to the repair of mismatched DNA, may have a key role in Huntington’s disease. The neurons that are impaired in Huntington’s are particularly susceptible to this mismatch damage that is not fixed. The findings have been reported in Cell.
In this work, the researchers used a mouse model of Huntington’s disease to study the impact of several genes on the disorder, including six genes related to DNA mismatch repair. In mice that were engineered to lack the mismatch repair genes Msh3 and Pms1, many of the symptoms of Huntington’s that these mice mimic were rescued. Some of the molecular and cellular pathology of Huntingon’s disease (HD) was no longer observed in the brains of these animals, and there were improvements in gait and movement.
ETH Zurich researchers have investigated how tiny gas bubbles can deliver drugs into cells in a targeted manner using ultrasound. For the first time, they have visualized how tiny cyclic microjets liquid jets generated by microbubbles penetrate the cell membrane, enabling the drug uptake.
The targeted treatment of brain diseases such as Alzheimer’s, Parkinson’s or brain tumors is challenging because the brain is a particularly sensitive organ that is well protected. That’s why researchers are working on ways of delivering drugs to the brain precisely, via the bloodstream. The aim is to overcome the blood–brain barrier, which normally only allows certain nutrients and oxygen to pass through.
Microbubbles that react to ultrasound are a particularly promising method for this sort of therapy. These microbubbles are smaller than a red blood cell, are filled with gas and have a special coating of fat molecules to stabilize them. They are injected into the bloodstream together with the drug and then activated at the target site using ultrasound. The movement of the microbubbles creates tiny pores in the cell membrane of the blood vessel wall that the drug can then pass through.
University of California, Los Angeles researchers have discovered that chronic stress flips brain activity between two amygdala-striatal pathways, disrupting flexible decision-making and promoting inflexible habits.
The research identifies distinct roles for the basolateral amygdala –dorsomedial striatum (BLA→DMS) and central amygdala–dorsomedial striatum (CeA→DMS) circuits in action-outcome learning and habit formation.
Chronic stress impairs goal-directed decision-making, often leading to rigid, habitual behaviors that underpin several psychiatric conditions. Understanding the neuronal circuits involved could illuminate vulnerabilities in disorders like substance use, obsessive-compulsive disorder, and depression.
Brain circuits are known to gradually form and develop after birth as the result of both innate biological processes and life experiences. Past studies suggest that the initial development of brain circuits spans across two different stages.
The first of these stages takes place before animals and humans start experiencing life. During this stage, the initial organization of cortical networks is established via internal (i.e., endogenous) mechanisms.
Following the formation of this initial organization, the second stage begins. This second phase entails the refinement of cortical networks over time in response to an animal or human’s individual life experiences.
This approach significantly enhances performance, as observed in Atari video games and several other tasks involving multiple potential outcomes for each decision.
“They basically asked what happens if rather than just learning average rewards for certain actions, the algorithm learns the whole distribution, and they found it improved performance significantly,” explained Professor Drugowitsch.
In the latest study, Drugowitsch collaborated with Naoshige Uchida, a professor of molecular and cellular biology at Harvard University. The goal was to gain a better understanding of how the potential risks and rewards of a decision are weighed in the brain.
Scientists are exploring gene editing as a way to correct trisomy at the cellular level. Using CRISPR-Cas9, researchers successfully removed extra copies of chromosome 21 in Down syndrome cell lines, restoring normal gene expression.
This breakthrough suggests that, with further development, similar approaches could be applied to neurons and glial cells, offering a potential treatment for those with the condition.
Gene Editing for Trisomy Treatment.
