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Bipolar disorder affects millions of Americans, causing dramatic swings in mood and, in some people, additional effects such as memory problems.

While bipolar disorder is linked to many genes, each one making small contributions to the disease, scientists don’t know just how those genes ultimately give rise to the disorder’s effects.

However, in new research, scientists at the University of Wisconsin-Madison have found for the first time that disruptions to a particular protein called Akt can lead to the brain changes characteristic of bipolar disorder. The results offer a foundation for research into treating the often-overlooked cognitive impairments of bipolar disorder, such as memory loss, and add to a growing understanding of how the biochemistry of the brain affects health and disease.

Gene editing has shown great promise as a non-heritable way to treat a wide range of conditions, including many genetic diseases and more recently, even COVID-19. But could a version of the CRISPR gene-editing tool also help deliver long-lasting pain relief without the risk of addiction associated with prescription opioid drugs?

In work recently published in the journal Science Translational Medicine, researchers demonstrated in mice that a modified version of the CRISPR system can be used to “turn off” a gene in critical neurons to block the transmission of pain signals [1]. While much more study is needed and the approach is still far from being tested in people, the findings suggest that this new CRISPR-based strategy could form the basis for a whole new way to manage chronic pain.

This novel approach to treating chronic pain occurred to Ana Moreno, the study’s first author, when she was a Ph.D. student in the NIH-supported lab of Prashant Mali, University of California, San Diego. Mali had been studying a wide range of novel gene-and cell-based therapeutics. While reading up on both, Moreno landed on a paper about a mutation in a gene that encodes a pain-enhancing protein in spinal neurons called NaV1.7.

Dr. Shawna Pandya MD, is a scientist-astronaut candidate with Project PoSSUM, physician, aquanaut, speaker, martial artist, advanced diver, skydiver, and pilot-in-training.

Dr. Pandya is also the VP of Immersive Medicine with the virtual reality healthcare company, Luxsonic Technologies, Director of the International Institute of Astronautical Sciences (IIAS)/PoSSUM Space Medicine Group, Chief Instructor of the IIAS/PoSSUM Operational Space Medicine course, Director of Medical Research at Orbital Assembly Construction (a company building the world’s first rotating space station providing the first artificial gravity habitat), clinical lecturer at the University of Alberta, podcast host with the World Extreme Medicine’s WEMCast series, Primary Investigator (PI) for the Shad Canada-Blue Origin student micro-gravity competition, member of the ASCEND 2021 Guiding Coalition, Life Sciences Team Lead for the Association of Spaceflight Professionals, sesional lecturer for the “Technology and the Future of Medicine,” course at the University of Alberta, and Fellow of the Explorers’ Club.

Dr. Pandya also serves as medical advisor to several space, medical and technology companies, including Mission: Space Food, Gennesys and Aquanauta, as well as the Jasper Dark Sky Festival Advisory Committee.

Dr. Pandya holds a Bsc degree in neuroscience from University of Alberta, a MSc in Space Studies from International Space University, an MD from University of Alberta, and a certification in entrepreneurship from the Graduate Studies Program at Singularity University.

Dr. Pandya is currently completing a fellowship in Wilderness Medicine (Academy of Wilderness Medicine), was granted an Honorary Fellowship in Extreme and Wilderness Medicine by the World Extreme Medicine organization in 2021, and was one of 50 physicians selected to attend the 2021 European Space Agency Space Medicine Physician Training Course. Dr. Pandya was named one of the Women’s Executive Network’s Top 100 Most Powerful Women in Canada in 2021, and a Canadian Space Agency Space Ambassador in 2021.

Dr. Pandya was part of the first crew to test a commercial spacesuit in zero-gravity in 2015. Dr. Pandya earned her aquanaut designation during the 2019 NEPTUNE (Nautical Experiments in Physiology, Technology and Underwater Exploration) mission. She previously served as Commander during a 2020 tour at the Mars Desert Research Station. Her expeditions were captured in the Land Rover short, released with the Apollo 11: First Steps film. She previously interned at ESA’s European Astronaut Center and NASA’s Johnson Space Center.

New data from Children’s National Hospital shows parental experience with a number of social determinants of health can ultimately impact brain development in utero, something researchers said should suggest future community health intervention among pregnant people. The data, published in JAMA Network Open, specifically found poorer brain development in fetuses among pregnant people with low socioeconomic status (SES), low educational attainment, and limited employment opportunity.


New data from Children’s National Hospital has found that social determinants of health like income, education, and occupation can impact fetal brain development, following that child into life.

As brain activity-dependent human genes are of great importance in human neuropsychiatric disorders we also examined the expression of these genes to postmortem RNAseq databases from patients suffering from various neurological and psychiatric disorders (Table 1). Datasets were chosen based on similarities in tissue processing and RNAseq methodology to our own protocol. We performed a PCA (Principal Component Analysis) of our fresh brain compared to postmortem brain from healthy, Parkinson’s, Schizophrenia, Huntington’s, and Autism brains for the top 500 brain activity-dependent genes that showed the greatest reduction in the healthy postmortem samples. The PCA revealed a significant separation between the 4 fresh samples and the postmortem samples, independent of whether or not the fresh tissue was from epileptic (high activity, H) or non-epileptic (low activity, L) brain regions (Fig. 2 J). This further demonstrates a selective reduction of activity-dependent genes in postmortem brain independent of whether the underlying tissue is electrically active or not.

The sudden removal of brain tissue from a living person in many ways mimics a catastrophic event that occurs with a hypoxic brain injury or a traumatic death with exsanguination. The human brain has high energy needs, estimated to be 10 times that of other tissues21. As a means to understand how the postmortem interval selectively affects some genes and not others in human neocortex, we performed RNAseq and histological analyses in cortical brain tissue as a function of time from 0–24 h at 24 °C in order to simulate a postmortem interval. Neuropathological examination of the tissue used for this study showed a normal-appearing cortical pattern with no histopathologic abnormalities. RNAseq analysis showed a loss of brain activity-dependent genes that were 3-times more prone to be degraded than expected by chance compared to more stable housekeeping genes (Table 2). The threshold to detect activity-dependent genes was related to the probability of being affected by the PMI. The higher the relative expression of the brain activity gene, the more it was enriched in the population of genes affected by the PMI. These findings confirm that genes involved in brain activity are more prone to degradation during the PMI.

One possible explanation for the selective loss of activity-dependent genes could relate to the stability of various cell populations during the simulated PMI. As a means to implicate specific cell populations that could be responsible for the reduction of genes during the simulated PMI we used a clustering algorithm as we have previously described9. We found that 1427 genes (71% known brain activity-dependent genes) could be clustered across the seven time points of the simulated PMI. For these clusters, we used AllegroMcode to identify two main clusters. One cluster of 317 rapidly declining genes was predicted to be neuronal and strongly overlapped with the activity-dependent genes. A second cluster of 474 genes was predicted to be glial, including astrocytes and microglia (Fig. 3A). Remarkably, as the neuronal cell cluster rapidly fell, there was a reciprocal and dramatic increase in the expression of the glial cell cluster (Fig. 3B).

Many of us have been wracking our brains why Nvidia would spend a fortune – a whopping $40 billion – to acquire Arm Holdings, a chip architecture licensing company that generates on the order of $2 billion in sales – since the deal was rumored back in July 2020. As we sat and listened to the Arm Vision Day rollout of the Arm V9 architecture, which will define processors ranging from tiny embedded controllers in IoT device all the way up to massive CPUs in the datacenter, we may have figured it out.

There are all kinds of positives, as we pointed out in our original analysis ahead of the deal, in our analysis the day the deal was announced in September 2020, and in a one-on-one conversation with Nvidia co-founder and chief executive officer Jensen Huang in October 2020.

We have said for a long time that we believe that Nvidia needs to control its own CPU future, and even joked with Huang that it didn’t need to have to buy all of Arm Holdings to make the best Arm server CPU, to which he responded that this was truly a once-in-a-lifetime opportunity to create value and push all of Nvidia’s technologies – its own GPUs for compute and graphics and Mellanox network interface chips, DPU processors, and switch ASICs – through an Arm licensing channel to make them all as malleable and yet standardized as the Arm licensing model not only allows, but encourages.

“Because contrast suppression is orientation-specific and relies on cortical processing, our results suggest that people experiencing a major depressive episode have normal retinal processing but altered cortical contrast normalization,” write the researchers in their paper.


We know that depression is linked to variations in the way our brains are wired, but new research suggests that people who are going through a depressive episode actually see the world around them differently.

And the team behind the study hopes that a better understanding of how visual information is processed in the brains of people with depression could help to inform our treatment approaches in the future.

The researchers wanted to analyze how the cerebral cortex – responsible for receiving messages from the five senses – handled an optical illusion, testing it out with 111 people who were experiencing major depressive episodes and 29 people who weren’t.

Sargramostim/GM-CSF is prescribed to boost white blood cells after cancer treatments or exposure to radiation. The protein stimulates the bone marrow to make more macrophages and granulocytes, specific types of white blood cells, and progenitor cells that repair blood vessels. These white blood cells circulate throughout the body and remove cells, bacteria and amyloid deposits and also repairing blood vessels.


The team carried out a randomized, double-blind, placebo-controlled Phase II trial (NCT01409915) to test the safety and efficacy of Sargramostim treatment in participants with mild-moderate Alzheimer’s disease.

Study participants were either administered Sargramostim at the standard FDA dose of 250 μg/m2/day by subcutaneous injection, or saline for five days a week for three weeks. The study included 20 participants in the test and placebo group. Most participants in the study were recruited and treated at CU Anschutz with a few from the University of South Florida. The CU Anschutz researchers then conducted and studied multiple neurological, neuropsychological, cell, cytokine, Alzheimer’s pathology biomarkers and neuroimaging assessments.

The investigators found that short-term Sargramostim treatment increased innate and other immune cells, modulated cytokine measures, and was safe and well-tolerated by participants. They also found cognition memory improved by almost two points in the 30 point Mini-Mental State Exam. Brain amyloid, tangles, neurodegeneration, and measures of blood biomarkers of Alzheimer’s disease, all improved toward normal.