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Category: biotech/medical – Page 794

In a world first, a quadriplegic man in the United States has regained touch and movement after surgeons successfully implanted microchips into his brain.

AI is then used to read, interpret and translate his thoughts into action.

Keith Thomas, 45, broke his neck in an accident and became paralysed from his chest down.

‘Fooling the nervous system to make it work’

Dr Ashesh Mehta, the surgeon who performed Thomas’ brain surgery said the wiring in Thomas’ brain was “broken”.

The surgical team had to rewire the pathways where electrical signals are sent between the brain, the body and the spinal cord.

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Low-grade inflammation contributes to age-related decline and impairment, but the precise pathways responsible for this inflammation and their impact on natural aging have until now remained elusive.

A study headed by researchers at the Swiss Federal Institute of Technology Lausanne (EPFL) has now shown that a molecular signaling pathway known as cGAS/STING plays a critical role in driving chronic inflammation and functional decline during aging. Andrea Ablasser, PhD, and colleagues found that blocking the STING protein suppressed inflammatory responses in human senescent cells and tissues, and reduced aging-related inflammation in multiple peripheral organs and in the brain in mice.

The researchers in addition studied the effects of blocking the STING protein in aged mice. As expected by its central role in driving inflammation, inhibiting STING alleviated markers of inflammation both in the periphery and in the brain. “Notably, various aging-related immune signature genes were significantly attenuated as a result of STING inhibition,” they stated. And importantly, animals receiving STING inhibitors displayed significant enhancements in spatial and associative memory, as well as improved muscle strength and physical endurance.

“Consistently, STING inhibition by H-151, a brain permeable compound, reduced the levels of immune-related signature genes in the brains of aged mice,” the scientists pointed out. “Together, these results establish STING as an important driver of aging-associated inflammation, both in the periphery and the CNS, promoting frailty and cognitive decline.”

The study advances our understanding of aging-related inflammation and also offers potential strategies for slowing cognitive deterioration in age-associated neurodegenerative conditions. The precise elucidation of the neuroimmune crosstalk governing microglial-dependent neurotoxicity also holds promise for the future study of neurodegenerative diseases. The team concluded, “Together with previous studies in models of Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and frontotemporal dementia, and Nieman–Pick’s disease, our study reveals notable convergence on cGAS–STING signaling in chronic neurodegenerative conditions … Our findings establish the cGAS–STING pathway as a driver of aging-related inflammation in peripheral organs and the brain, and reveal blockade of cGAS–STING signaling as a potential strategy to halt neurodegenerative processes during old age.”

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New research on mice has shed light on how high blood pressure causes changes to arteries in the brain, a process that leads to vascular dementia. The research, led by University of Manchester scientists, funded by the British Heart Foundation and published today in the journal Proceedings of the National Academy of Sciences, [1] has uncovered a route to developing the first ever drug treatments for vascular dementia that directly target a cause of the condition.

High blood pressure is the main cause of vascular dementia, a condition characterised by poor blood flow to the brain. The reduced blood supply starves brain cells of nutrients and over time they become damaged and die. Symptoms of vascular dementia include loss of energy, lack of concentration and poor memory.

It’s normal for the brain’s arteries to narrow and widen in response to changes in blood pressure. However, consistently high blood pressure causes arteries to stay narrow and restrict the brain’s blood supply. Until now, it was not known why.

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Researchers have identified two ion channel switches that regulate the release of dopamine in the brain, a first step that might one day lead to therapeutics for a wide range of diseases and disorders that currently have few solutions.

The switches help regulate learning and motivational state in mice. Humans also have hundreds of these channels, which govern many chemical and hormonal processes that influence behavior and mood. The University of Washington School of Medicine research team hopes to identify drugs to target these channels. Those drug candidates could then be tested in clinical trials.

“The ability to precisely manipulate how dopamine-producing neurons of the brain regulate different behaviors is a major step toward developing better therapies for a range of mental illnesses,” said Larry Zweifel, professor of psychiatry & behavioral sciences at the UW School of Medicine.

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The findings were published Aug. 10 in the journal Nature Neuroscience.

“It’s amazing that children with the same symptoms end up with two distinct forms of altered neural networks,” said Dr. Flora Vaccarino, the Harris Professor in the Child Study Center at Yale School of Medicine and co-senior author of the paper.

Two distinct neurodevelopmental abnormalities that arise just weeks after the start of brain development have been associated with the emergence of autism spectrum disorder, according to a new Yale-led study in which researchers developed brain organoids from the stem cells of boys diagnosed with the disorder.

And, researchers say, the specific abnormalities seem to be dictated by the size of the child’s brain, a finding that could help doctors and researchers to diagnosis and treat autism in the future.

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A form of gene therapy currently used to treat Parkinson’s disease may dramatically reduce alcohol use among chronic heavy drinkers, researchers at Oregon Health & Science University and institutions across the country have found.

The study in nonhuman primates showed that implanting a specific type of molecule that induces cell growth effectively resets the brain’s dopamine reward pathway in animals predisposed to heavy drinking. The gene therapy procedure involves brain surgery, and may be useful in the most severe cases of alcohol use disorder.

Already used in clinical trials to treat Parkinson’s disease, OHSU researchers found surgical treatment dramatically reduced chronic heavy drinking.

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In a groundbreaking study published today in Nature, Australian scientists have resolved a long-standing problem in regenerative medicine. Led by Professor Ryan Lister from the Harry Perkins Institute of Medical Research and The University of Western Australia and Professor Jose M Polo from Monash University and the University of Adelaide, the team developed a new method to reprogram human cells to better mimic embryonic stem cells, with significant implications for biomedical and therapeutic uses.

In a revolutionary advance in the mid-2000s, it was discovered that the non-reproductive adult cells of the body, called ‘somatic’ cells, could be artificially reprogrammed into a state that resembles embryonic stem (ES) cells which have the capacity to then generate any cell of the body.

The ability to artificially reprogram human somatic cells, such as skin cells, into these so-called induced pluripotent stem (iPS) cells provided a way to make an essentially unlimited supply of ES-like cells, with widespread applications in disease modelling, drug screening and cell-based therapies.

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A protein involved in wound healing can improve learning and memory in ageing mice1.

Platelet factor 4 (PF4) has long been known for its role in promoting blood clotting and sealing broken blood vessels. Now, researchers are wondering whether this signalling molecule could be used to treat age-related cognitive disorders such as Alzheimer’s disease.

“The therapeutic possibilities are very exciting,” says geneticist and anti-ageing scientist David Sinclair at Harvard University in Boston, Massachusetts, who was not involved in the research. The study was published on 16 August in Nature.

Young blood, old brains.

A platelet factor joins the list of blood components that might have anti-ageing effects.

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Free will?

Neuroscientists and psychologists have been trying for decades to better understand how humans make decisions, in the hope to devise more effective interventions to promote healthy and beneficial lifestyle choices. Two brain regions that have been linked to decision-making are the orbitofrontal cortex (OFC) and the anterior cingulate cortex (ACC).

Researchers at University of California, Berkeley (UC Berkeley), have been conducting extensive research focusing on these two areas of the brain and exploring their involvement in . In a recent paper published in Nature Neuroscience, they presented interesting new findings that could shed light on the through which the brain prepares to make choices.

“We previously used neural recordings to determine what was going on during decision-making,” Joni Wallis, one of the researchers who carried out the study, told Medical Xpress. “We showed that OFC neurons represent the value of the options under consideration and flip-flopping them back and forth representing the value of each option in turn, as though the OFC is weighing up the two options. This flip-flopping predicts decision making: the more flip-flopping, the more likely the subject is to make a suboptimal choice or to take a long time over their decision.”

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This is a significant development that brings hope to the one billion individuals with obesity worldwide. Researchers led by Director C. Justin LEE from the Center for Cognition and Sociality (CCS) within the Institute for Basic Science (IBS) have discovered new insights into the regulation of fat metabolism. The focus of their study lies within the star-shaped non-neuronal cells in the brain, known as ‘astrocytes’. Furthermore, the group announced successful animal experiments using the newly developed drug ‘KDS2010’, which allowed the mice to successfully achieve weight loss without resorting to dietary restrictions.

The complex balance between food intake and energy expenditure is overseen by the hypothalamus in the brain. While it has been known that the neurons in the lateral hypothalamus are connected to fat tissue and are involved in fat metabolism, their exact role in fat metabolism regulation has remained a mystery. The researchers discovered a cluster of neurons in the hypothalamus that specifically express the receptor for the inhibitory neurotransmitter ‘GABA (Gamma-Aminobutyric Acid)’. This cluster has been found to be associated with the α5 subunit of the GABAA receptor and was hence named the GABRA5 cluster.

In a diet-induced obese mouse model, the researchers observed significant slowing in the pacemaker firing of the GABRA5 neurons. Researchers continued with the study by attempting to inhibit the activity of these GABRA5 neurons using chemogenetic methods. This in turn caused a reduction in heat production (energy consumption) in the brown fat tissue, leading to fat accumulation and weight gain. On the other hand, when the GABRA5 neurons in the hypothalamus were activated, the mice were able to achieve a successful weight reduction. This suggests that the GABRA5 neurons may act as a switch for weight regulation.

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