Lifeboat Foundation

Just as it’s hard to understand a conversation without knowing its context, it can be difficult for biologists to grasp the significance of gene expression without knowing a cell’s environment. To solve that problem, researchers at Princeton Engineering have developed a method to elucidate a cell’s surroundings so that biologists can make more meaning of gene expression information.

The researchers, led by Professor of Computer Science Ben Raphael, hope the new system will open the door to identifying rare cell types and choosing cancer treatment options with new precision. Raphael is the senior author of a paper describing the method published May 16 in Nature Methods.

The basic technique of linking gene expression with a cell’s environment, called spatial transcriptomics (ST), has been around for several years. Scientists break down tissue samples onto a microscale grid and link each spot on the grid with information about gene expression. The problem is that current computational tools can only analyze spatial patterns of gene expression in two dimensions. Experiments that use multiple slices from a single tissue sample—such as a region of a brain, heart or tumor—are difficult to synthesize into a complete picture of the cell types in the tissue.

Summary: Researchers have designed a new method of converting non-neural cells into functioning neurons that are able to form synapses, dispense dopamine, and restore the function of neurons undermined by Parkinson’s associated destruction of dopaminergic cells.

Neurodegenerative diseases damage and destroy neurons, ravaging both mental and physical health. Parkinson’s disease, which affects over 10 million people worldwide, is no exception. The most obvious symptoms of Parkinson’s disease arise after the illness damages a specific class of neuron located in the midbrain. The effect is to rob the brain of dopamine—a key neurotransmitter produced by the affected neurons.

In new research, Jeffrey Kordower and his colleagues describe a process for converting non-neuronal cells into functioning neurons able to take up residence in the brain, send out their fibrous branches across neural tissue, form synapses, dispense dopamine and restore capacities undermined by Parkinson’s destruction of dopaminergic cells.

Jesper AndersonNo. Nobody can “leave their body”. There is no evidence what so ever that this is possible.

What can be done is, copy many of your attributes and create a copy which behaves very much like you. But that’s simply an advanced method of writing a book. I… See more.

Craig Everett JonesAlthough neurons are much like transistors, our emotions are not just ones and zeroes. We feel things in our gut. I think singularity fans are grossly underestimating the dependencies between human consciousness and organic physiology. And, your b… See more.

Continue reading “COVID-19 in 2022—The Beginning of the End or the End of the Beginning?” »

How psilocybin evolved has more to do with sending insects on terrifying trips than it does making Phish sound good.

Research by Dr. Silvia de Santis and Dr. Santiago Canals, both from the Institute of Neurosciences UMH-CSIC (Alicante, Spain), has made it possible to visualize for the first time and in great detail brain inflammation using diffusion-weighted Magnetic Resonance Imaging. This detailed “X-ray” of inflammation cannot be obtained with conventional MRI, but requires data acquisition sequences and special mathematical models. Once the method was developed, the researchers were able to quantify the alterations in the morphology of the different cell populations involved in the inflammatory process in the brain.

An innovative strategy developed by the researchers has made possible this important breakthrough, which is published today in the journal Science Advances and which may be crucial to change the course of the study and treatment of neurodegenerative diseases.

The research demonstrates that diffusion-weighted MRI can noninvasively and differentially detect the activation of microglia and astrocytes, two types of brain cells that are at the basis of neuroinflammation and its progression.

Summary: Muffled sounds experienced in the womb prime the brain’s ability to interpret some sounds and may be key for auditory development.

Source: MIT

Inside the womb, fetuses can begin to hear some sounds around 20 weeks of gestation. However, the input they are exposed to is limited to low-frequency sounds because of the muffling effect of the amniotic fluid and surrounding tissues.

The Stem Cell Reports paper demonstrated the capability to grow and differentiate cortical neurons — known to be responsible for a majority of higher brain function — into fully mature and functional cells.

These neurons were then incorporated into a circuit functioning as a simulated system, where the researchers were able to induce long-term potentiation (LTP). LTP — which allows for memory formation — is a key phenomenon in the study of cognition, and one that has mostly evaded direct observation in human models.

A UCF researcher’s work to create a “brain-on-a-chip” aims to improve neurological disorder research by speeding up drug discovery and providing an alternative to animal testing.

Continue reading “‘Brain-on-a-Chip’ Technology Advances Toward a New Form of Drug Screening” »

Most treatments for strokes aim to help reduce or repair damage to affected neurons. But a new study in mice has shown that a drug already in use to treat certain neurological disorders could help patients recover from strokes by getting undamaged neurons to pick up the slack.

An ischemic stroke occurs when a blood vessel blockage interrupts blood flow to the brain, causing neurons to die off. Survivors can suffer impaired fine motor control and speech, and other disabilities, for which long-term rehabilitation is often required.

Logically, many treatment options in development focus on minimizing or reversing damage to neurons, using things like stem cells, anti-inflammatory drugs, injectable hydrogels, or molecules that convert neighboring cells into neurons.

Repression of the G protein-coupled chemokine receptor CCR5 enhances MAPK/CREB signaling, long-term potentiation, somatosensory cortical plasticity, and learning and memory, while CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits.