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The continuing miniaturization of electronics is opening up some exciting possibilities when it comes to what we might place in our bodies to monitor and improve our health. Engineers at Columbia University have demonstrated an extreme version of this technology, developing the smallest single-chip system ever created, which could be implanted with a hypodermic needle to measure temperature inside the body, and possibly much more.

From ladybug-sized implants that track oxygen levels in deep body tissues to tiny “neural dust” sensors that monitor nerve signals in real time, scientists are making big steps when it comes to the functionality of tiny electronic devices. The implant developed by the Columbia Engineers breaks new ground as the world’s smallest single-chip system, which is a completely functional electronic circuit with a total volume of less than 0.1 mm3.

That makes it as small as a dust mite, and only visible under a microscope. The tiny chip required some outside-the-box thinking to make, particularly when it comes to the way it communicates and is powered.

In our ongoing search to continuously improve our health, we occasionally pay lip service to the bacteria that live inside our gut. Normally this concern rarely manifests as anything more than occasionally remembering to buy some of those small bottles of pro-biotic yoghurts while shopping for your…


Recent discoveries have led to the conclusion that the gut plays an important role in cognitive function, with a large amount of research into understanding what is known as the gut-brain axis, which is the collective name given to the biochemical signalling pathways which take place between the gastrointestinal tract and the central nervous system. With an ever-increasing understanding of this pathway, along with an expanded understand of the gut flora (which was found to decline with age), researchers started to ask how the gut flora are involved in the ageing process.

In order to test how exactly ageing gut flora effects the gut-brain axis, researchers at the University of East Anglia conducted a faecal transplant from elderly mice into younger mice. Following this transplant, the young mice were then put through a serious of tests to assess their cognitive abilities. The younger mice showed significant changes in their microbial profiles, as well as significantly impaired capacity for spatial learning, as well as a decreased capacity for memorisation. These mice also showed an altered expression of proteins associated with neurotransmission and neuroplasticity, along with changes in the mice’s hippocampus, which is responsible for allowing the mice to memories new information, as well as recalling previous memories.

This research has successfully proven a link between the changing microbiome of the gut and protein expression within the central nervous system. This discovery is exceptionally good news, as not only is the problem potentially fairly easy to fix (with an aforementioned faecal transplant), but it also provides clues as to how we might compensate for this age related change in the gut microbiome with medication tailors to mimic the role of a young microbiome. Either way, the discovery has opened the door to a number of exciting prospects for regenerative medicine, along with maybe highlighting the fact that we should really start considering our gut bacteria as more than just a collection of microorganisms, and more of a collection of symbiotic organisms that benefit us in ways that we are only just beginning to understand.

In a major breakthrough, researchers at Massachusetts General Hospital (MGH) have discovered how amyloid beta—the neurotoxin believed to be at the root of Alzheimer’s disease (AD)—forms in axons and related structures that connect neurons in the brain, where it causes the most damage. Their findings, published in Cell Reports, could serve as a guidepost for developing new therapies to prevent the onset of this devastating neurological disease.

Among his many contributions to research on AD, Rudolph Tanzi, Ph.D., vice chair of Neurology and co-director of the McCance Center for Brain Health at MGH, led a team in 1986 that discovered the first Alzheimer’s disease gene, known as APP, which provides instructions for making protein precursor (APP). When this protein is cut (or cleaved) by enzymes—first, beta secretase, followed by gamma secretase—the byproduct is amyloid beta (sometimes shortened to Abeta). Large deposits of amyloid beta are believed to cause neurological destruction that results in AD. Amyloid beta formed in the brain’s axons and nerve endings causes the worst damage in AD by impairing communication between nerve cells (or neurons) in the brain. Researchers around the world have worked intensely to find ways to block the formation of amyloid beta by preventing cleavage by beta secretase and gamma secretase. However, these approaches have been hampered by safety issues.

Despite years of research, a major mystery has remained. “We knew that Abeta is made in the axons of the brain’s nerve cells, but we didn’t know how,” says Tanzi. He and his colleagues probed the question by studying the brains of mice, as well as with a research tool known as Alzheimer’s in a dish, a three-dimensional cell culture model of the disease created in 2014 by Tanzi and a colleague, Doo Yeon Kim, Ph.D. Earlier, in 2013, several other MGH researchers, including neurobiologist Dora Kovacs, Ph.D. (who is married to Tanzi), and Raja Bhattacharyya, Ph.D., a member of Tanzi’s lab, showed that a form of APP that has undergone a process called palmitoylation (palAPP) gives rise to amyloid beta. That study indicated that, within the neuron, palAPP is transported in a fatty vesicle (or sac) known as a lipid raft. But there are many forms of lipid rafts.

Researchers with the BrainGate Collaboration have deciphered the brain activity associated with handwriting: working with a 65-year-old (at the time of the study) participant with paralysis who has sensors implanted in his brain, they used an algorithm to identify letters as he attempted to write them; then, the system displayed the text on a screen; by attempting handwriting, the participant typed 90 characters per minute — more than double the previous record for typing with a brain-computer interface.

So far, a major focus of brain-computer interface research has been on restoring gross motor skills, such as reaching and grasping or point-and-click typing with a computer cursor.

Scientists modify CAR T-Cell therapy, making it more effective and less toxic, for possible use in solid tumors such as neuroblastoma.


Chimeric Antigen Receptor T-cell therapy — CAR T — has revolutionized leukemia treatment. Unfortunately, the therapy has not been effective for treating solid tumors including childhood cancers such as neuroblastoma. Preclinical studies using certain CAR T against neuroblastoma revealed toxic effects. Now, a group of scientists at Children’s Hospital Los Angeles have developed a modified version of CAR T that shows promise in targeting neuroblastoma, spares healthy brain tissue and more effectively kills cancer cells. Their study was published today in Nature Communications. While this work is in the preclinical phase, it reveals potential for lifesaving treatment in children and adults with solid tumors.

Shahab Asgharzadeh, MD, a physician scientist at the Cancer and Blood Disease Institute of CHLA, is working to improve the lifesaving CAR T-cell therapy, in which scientists take a patient’s own immune system T-cells and engineer them to recognize and destroy cancer cells.

“The CAR T therapy works in leukemia,” he says, “by targeting a unique protein (or antigen) on the surface of leukemia cells. When the treatment is given, leukemia cells are killed. CAR T turns the patient’s immune system into a powerful and targeted cancer-killer in patients with leukemia. This antigen is also on normal B cells in the blood, but this side effect can be treated medically.”

And cells from people with mutations in KMT2D, which results in Kabuki syndrome, showed similar patterns of activity to the EHMT1 cells. Kabuki syndrome often results in intellectual disability but is not typically linked to autism.

Cells that carry mutations in ARID1B showed a distinct pattern of network activity, with short, small bursts occurring at an unusually high rate.

Moving forward, Nadif Kasri and his colleagues plan to test other genes that increase a person’s likelihood of being autistic. They also plan to explore how these activity patterns compare at the individual level, and how they relate to other autism-linked traits, he says.

Criticism of a recent video denouncing resveratrol.


Following Doctor Brad Stanfield’s latest ‘why I stopped video’, this last one about resveratrol and pterostilbene, many of you asked for my opinion, well here it is.

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Humans are distinguished from other species by several aspects of cognition. While much comparative evolutionary neuroscience has focused on the neocortex, increasing recognition of the cerebellum’s role in cognition and motor processing has inspired considerable new research. Comparative molecular studies, however, generally continue to focus on the neocortex. We sought to characterize potential genetic regulatory traits distinguishing the human cerebellum by undertaking genome-wide epigenetic profiling of the lateral cerebellum, and compared this to the prefrontal cortex of humans, chimpanzees, and rhesus macaque monkeys. We found that humans showed greater differential CpG methylation–an epigenetic modification of DNA that can reflect past or present gene expression–in the cerebellum than the prefrontal cortex, highlighting the importance of this structure in human brain evolution. Humans also specifically show methylation differences at genes involved in neurodevelopment, neuroinflammation, synaptic plasticity, and lipid metabolism. These differences are relevant for understanding processes specific to humans, such as extensive plasticity, as well as pronounced and prevalent neurodegenerative conditions associated with aging.

Citation: Guevara EE, Hopkins WD, Hof PR, Ely JJ, Bradley BJ, Sherwood CC (2021) Comparative analysis reveals distinctive epigenetic features of the human cerebellum. PLoS Genet 17: e1009506. https://doi.org/10.1371/journal.pgen.

Editor: Takashi Gojobori, National Institute of Genetics, JAPAN.