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Summary: Tau spreads through the human brain via neural communication pathways. The spread is accelerated by the presence of amyloid-beta.

Source: Lund University

Toxic versions of the protein tau are believed to cause death of neurons of the brain in Alzheimer’s disease. A new study published in Nature Communications shows that the spread of toxic tau in the human brain in elderly individuals may occur via connected neurons. The researchers could see that beta-amyloid facilitates the spread of toxic tau.

August 19, 2019 — An international team of researchers developed a new magnetic resonance imaging (MRI) technique that can capture an image of a brain thinking by measuring changes in tissue stiffness. The results show that brain function can be tracked on a time scale of 100 milliseconds – 60 times faster than previous methods. The technique could shed new light on altered neuronal activity in brain diseases.

The human brain responds almost immediately to stimuli, but non-invasive imaging techniques haven’t been able to keep pace with the brain. Currently, several non-invasive brain imaging methods measure brain function, but they all have limitations. Most commonly, clinicians and researchers use functional magnetic resonance imaging (fMRI) to measure brain activity via fluctuations in blood oxygen levels. However, a lot of vital brain activity information is lost using fMRI because blood oxygen levels take about six seconds to respond to a stimulus.

Since the mid-1990s, researchers have been able to generate maps of tissue stiffness using an MRI scanner, with a non-invasive technique called magnetic resonance elastography (MRE). Tissue stiffness can not be measured directly, so instead researchers use MRE to measure the speed at which mechanical vibrations travel through tissue. Vibrations move faster through stiffer tissues, while vibrations travel through softer tissue more slowly; therefore, tissue stiffness can be determined. MRE is most commonly used to detect the hardening of liver tissue but has more recently been applied to other tissues like the brain.

Summary: Exposure to anesthesia causes lipid clusters to move from an ordered state to a disordered one, then back again. These changes lead to subsequent effects that cause changes in consciousness.

Source: Scripps Research Institute

Surgery would be inconceivable without general anesthesia, so it may come as a surprise that despite its 175-year history of medical use, doctors and scientists have been unable to explain how anesthetics temporarily render patients unconscious.

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Today and going forward, billions of tiny devices will act as an extension of our brains, feelings and emotions as a natural extension of everyday life.

In addition, the mice developed interstitial pneumonia, which affects the tissue and space around the air sacs of the lungs, causing the infiltration of inflammatory cells, the thickening of the structure that separates air sacs, and blood vessel damage. Compared with young mice, older mice showed more severe lung damage and increased production of signaling molecules called cytokines. Taken together, these features recapitulate those observed in COVID-19 patients.

When the researchers administered SARS-CoV-2 into the stomach, two of the three mice showed high levels of viral RNA in the trachea and lung. The S protein was also present in lung tissue, which showed signs of inflammation. According to the authors, these findings are consistent with the observation that patients with COVID-19 sometimes experience gastrointestinal symptoms such as diarrhea, abdominal pain, and vomiting. But 10 times the dose of SARS-CoV-2 was required to establish infection through the stomach than through the nose.

Future studies using this mouse model may shed light on how SARS-CoV-2 invades the brain and how the virus survives the gastrointestinal environment and invades the respiratory tract. “The hACE2 mice described in our manuscript provide a small animal model for understanding unexpected clinical manifestations of SARS-CoV-2 infection in humans,” concluded co-senior study author Chang-Fa Fan of NIFDC. “This model will also be valuable for testing vaccines and therapeutics to combat SARS-CoV-2.”

Subtle patterns can be seen in people’s reaction times as their memories are recalled, and boosting these brainwaves could help treat Alzheimer’s disease.

Although we often think of knowledge as “knowing that” (for example, knowing that Paris is the capital of France), each of us also knows many procedures consisting of “knowing how,” such as knowing how to tie a knot or start a car. Now, a new study has found the brain programs that code the sequence of steps in performing a complex procedure.

In a just published paper in Psychological Science, researchers at Carnegie Mellon University have found a way to find decode the procedural information required to tie various knots with enough precision to identify which knot is being planned or performed. To reach this conclusion, Drs. Robert Mason and Marcel Just first trained a group of participants to tie seven types of knots, and then scanned their brains while they imagined tying, or actually tied the knots while they were in an MRI scanner. The main findings were that each knot had a distinctive neural signature, so the researchers could tell which knot was being tied from the sequence of brain images collected. Furthermore, the neural signatures were very similar for imagining tying a particular knot and planning to tie it.

Dr. Just said, “Tying a knot is an ancient and frequently performed human action that is the epitome of everyday procedural knowledge, making it an excellent target for investigation.”

Episodic memory requires linking events in time, a function dependent on the hippocampus. In “trace” fear conditioning, animals learn to associate a neutral cue with an aversive stimulus despite their separation in time by a delay period on the order of tens of seconds. But how this temporal association forms remains unclear. Here we use two-photon calcium imaging of neural population dynamics throughout the course of learning and show that, in contrast to previous theories, hippocampal CA1 does not generate persistent activity to bridge the delay. Instead, learning is concomitant with broad changes in the active neural population. Although neural responses were stochastic in time, cue identity could be read out from population activity over longer timescales after learning. These results question the ubiquity of seconds-long neural sequences during temporal association learning and suggest that trace fear conditioning relies on mechanisms that differ from persistent activity accounts of working memory.