Lifeboat Foundation

Writing in Nature Medicine, an international team headed by researchers at University of California San Diego School of Medicine describe a new way to effectively deliver a gene-silencing vector to adult amyotrophic lateral sclerosis (ALS) mice, resulting in long-term suppression of the degenerative motor neuron disorder if treatment vector is delivered prior to disease onset, and blockage of disease progression in adult animals if treatment is initiated when symptoms have already appeared.

The findings are published in the December 23, 2019 online issue of the journal Nature Medicine. Martin Marsala, MD, professor in the Department of Anesthesiology at UC San Diego School of Medicine and a member of the Sanford Consortium for Regenerative Medicine, is senior author of the study.

ALS is a neurodegenerative disease that affects nerve cells in the brain and spinal cord. Motor neurons responsible for communicating movement are specifically harmed, with subsequent, progressive loss of muscle control affecting the ability to speak, eat, move and breathe. More than 5,000 Americans are diagnosed with ALS each year, with an estimated 30,000 persons currently living with the disease. While there are symptomatic treatments for ALS, there is currently no cure. The majority of patients succumb to the disease two to five years after diagnosis.

Dr Shima Beigi BSc, MSc, MSc, Ph.D. founder of Mindfulness Engineering™️ and ideaXme Rich Connectedness™️ ambassador interviews Dr Jon Finn founder Tougher Minds.

Dr Jon Finn:

Continue reading “How To Build A Tougher Mind: Dr Jon Finn” »

Talk with an Alzheimer’s researcher and you’ll likely hear the same lament: Finding a treatment or cure is incredibly challenging because scientists are not even certain what exactly causes the neurological disease in the first place.

In fact, researchers speak of a “web of causation” that can lead to Alzheimer’s. In addition to genetics, scientists look to so-called lifestyle elements such as blood pressure and blood sugar levels. Even the bacteria that live in our mouths are being scrutinized for their potential role in Alzheimer’s.

One element that researchers are completely certain about is that people who carry the apolipoprotein E4 gene — known as APOE4 — are at a greater risk of developing Alzheimer’s.

Lab-grown brain organoids developed from a patient’s own glioblastoma, the most aggressive and common form of brain cancer, may hold the answers on how to best treat it. A new study in Cell from researchers at Penn Medicine showed how glioblastoma organoids could serve as effective models to rapidly test personalized treatment strategies.

Glioblastoma multiforme (GBM) remains the most difficult of all brain cancers to study and treat, largely because of tumor heterogeneity. Treatment approaches, like surgery, radiation and chemotherapy, along with newer personalized cellular therapies, have proven to slow tumor growth and keep patients disease-free for some periods of time; however, a cure remains elusive.

“While we’ve made important strides in glioblastoma research, preclinical and clinical challenges persist, keeping us from getting closer to more effective treatments,” said senior author Hongjun Song, Ph.D., Perelman Professor of Neuroscience in the Perelman School of Medicine at the University of Pennsylvania. “One hurdle is the ability to recapitulate the tumor to not only better understand its complex characteristics, but also to determine what therapies post-surgery can fight it in a timelier manner.”

Has anybody else notice the light spectrum in new imaging. Color equals light frequency. This should be a major study. This vid is just for the color imagings reference.

In this informative talk about brain health, Dr. Daniel G. Amen makes a powerful case for preventative living through healthy habits. In a time where bodies are expanding and brains are shrinking, he calls this game-changing lifestyle The Brain Warrior’s Way.

Continue reading “How Dr. Daniel Amen Repairs the Brain with Healthy Living” »

Fossils of just about everything have been unearthed, from ancient feathers to entire dinosaur skeletons preserved in opal, but there is one thing nobody thought could survive hundreds of thousands of years—until now.

Brain matter from a Cambrian arthropod that crawled around 500,000 years ago has proven many paleontologists wrong about brain decay being inevitable. Previous research suggests that no matter what it may be protected by, soft neural matter will break down long before fossilization can even start. Minds have suddenly been changed. Alalcomenaeus may have been a tiny creature, but its exoskeleton was tough enough to ward off decomposition.

A new film, I AM HUMAN, explores the state of neurotechnology today: Its challenge, promise, and the issues it raises.

Researchers at Karolinska Institutet have come one step closer toward understanding how the part of our brain that is central for decision-making and the development of addiction is organized on a molecular level. In mouse models and with methods used for mapping cell types and brain tissue, the researchers were able to visualize the organization of different opioid-islands in striatum. Their spatiomolecular map, published in the journal Cell Reports, may further our understanding of the brain’s reward-system.

Striatum is the inner part of the brain that among other things regulates rewards, motivation, impulses and motor function. It is considered central to decision-making and the development of various addictions.

In this study, the researchers created a molecular 3D-map of the nerve cells targeted by opioids, such as morphine and heroin, and showed how they are organized in striatum. It is an important step toward understanding how the brain’s network governing motivation and drug addiction is organized. In the study, the researchers described a spatiomolecular code that can be used to divide striatum into different subregions.

Neurochemicals such as serotonin and dopamine play crucial roles in cognitive and emotional functions of our brain. Vesicular monoamine transporter 1 (VMAT1) is one of the genes responsible for transporting neurotransmitters and regulating neuronal signaling. A research team led by Tohoku University has reconstructed ancestral VMAT1 proteins, revealing the functional changes in neurotransmitter uptake of VMAT1 throughout the course of human evolution.

Human bodies are made up of millions of cells. Each individual contains a specific set of instruction of codes that make up all of a living thing’s genetic material. These instructions are known as genomes. PhD candidate Daiki Sato and Professor Masakado Kawata of the Graduate School of Life Sciences at Tohoku University, and two of the authors involved in the current study, previously discovered VMAT1 to be one of the genes that had evolved throughout human lineage.

VMAT 1 contains two human-specific mutations, or where the genomes changed, with the change being represented as 130Glu to 130Gly and from 136Asn to 136Thr. Previous studies have shown that having the new 130Gly/136Thr variant decreases the uptake of neurotransmitters and is associated with higher depression and/or anxiety. In this study, Sato, Kawata and their colleagues revealed the evolutionary changes in neurotransmitter uptake of VMAT1 by reconstructing ancestral VMAT1 proteins. First they applied a fluorescent substrate to visualize and quantify the neurotransmitter uptake of each genotype. The ancestral (130Glu/136Asn) VMAT1 protein exhibited an increased uptake of neurotransmitters compared to a derived (130Gly/136Thr) genotype. Given that the derived (130Gly/136Thr) genotype is shown to be associated with depression and/or anxiety in modern human populations. “This results of our study reveal that our ancestors may have been able to withstand higher levels of anxiety or depression,” noted the authors.

Continue reading “Evolutionary Changes in Brain Potentially Make us More Prone to Anxiety” »