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Category: neuroscience – Page 93

Leucovorin may help with improving verbal communication in certain individuals with ASD who have a vitamin deficiency

I think Paul may have posted this already, if so here is some more information from a site about drug repurposng. Its really cool.

Click the video above to watch a story that ran on CBS Evening News about leucovorin for ASD.

Every Cure is excited to highlight the potential role that leucovorin (folinic acid) may play in improving verbal communication in some individuals with autism spectrum disorder (ASD) who have speech challenges and certain antibodies that cause a vitamin deficiency in the brain. As a nonprofit research organization committed to identifying and elevating potential repurposed treatments, we’ve summarized information about this promising drug repurposing opportunity below.

A vitamin deficiency may contribute to speech challenges in some individuals with ASD.

ITSN1 gene linked to substantial risk of Parkinson’s disease

A new study published in Cell Reports reveals a breakthrough discovery linking genetic variants in the gene ITSN1 to a significantly elevated risk of Parkinson’s disease, a neurodegenerative condition that affects nearly 2% of adults older than 65 years.

These findings were subsequently validated across three independent cohorts comprising more than 8,000 cases and 400,000 controls. Importantly, ITSN1 carriers trended toward earlier age of disease onset.

ITSN1 plays an important role in how neurons send messages to each other – a process called synaptic transmission – making it particularly relevant to Parkinson’s disease, a condition in which disruption of nerve signals leads to the typical symptoms of impaired gait and balance, tremors and rigidity. “We also showed in fruit flies that reducing ITSN1 levels worsens Parkinson’s-like features, including the ability to climb. We plan to extend these investigations to stem cell and mouse models,” the author said.

Interestingly, previous studies have recently implicated similar ITSN1 mutations in autism spectrum disorder (ASD). Other emerging data also have suggested an association between ASD and Parkinson’s disease, indicating that people with ASD are three times more likely to develop parkinsonism.

Scientists Found The Silent ‘Scream’ of Human Skin For The First Time

The body you inhabit is made up of lots of moving parts that need to communicate with each other.

Some of this communication – in the nervous system, for example – takes the form of bioelectrical signals that propagate through the body to trigger the appropriate response.

Now, US researchers have discovered that the epithelial cells that line our skin and organs are able to signal the same way to communicate peril. They just use a long, slow ‘scream’, rather than the rapid-fire communication of neurons.

Bacteria invasion of brain after implants threatens long-term device effectiveness, research finds

Brain implants hold immense promise for restoring function in patients with paralysis, epilepsy and other neurological disorders. But a team of researchers at Case Western Reserve University has discovered that bacteria can invade the brain after a medical device is implanted, contributing to inflammation and reducing the device’s long-term effectiveness.

The research, published in Nature Communications, could improve the long-term success of brain implants now that a target has been identified to address.

“Understanding the role of bacteria in implant performance and brain health could revolutionize how these devices are designed and maintained,” said Jeff Capadona, Case Western Reserve’s vice provost for innovation, the Donnell Institute Professor of Biomedical Engineering and senior research career scientist at the Louis Stokes Cleveland VA Medical Center.

The emerging armamentarium of cognitive warfare with Dr. James Giordano | CSI Talks #19

Convergent engagement of neural and computational sciences and technologies are reciprocally enabling rapid developments in current and near-future military and intelligence operations. In this podcast, Prof. James Giordano of Georgetown University will provide an overview of how these scientific and technological fields can be — and are being — leveraged for non-kinetic and kinetic what has become known as cognitive warfare; and will describe key issues in this rapidly evolving operational domain.

James Giordano PhD, is the Pellegrino Center Professor in the Departments of Neurology and Biochemistry; Chief of the Neuroethics Studies Program; Co-director of the Project in Brain Sciences and Global Health Law and Policy; and Chair of the Subprogram in Military Medical Ethics at Georgetown University Medical Center, Washington DC. Professor Giordano is Senior Bioethicist of the Defense Medical Ethics Center, and Adjunct Professor of Psychiatry at the Uniformed Services University of Health Sciences; Distinguished Stockdale Fellow in Science, Technology, and Ethics at the United States Naval Academy; Senior Science Advisory Fellow of the SMA Branch, Joint Staff, Pentagon; Non-resident Fellow of the Simon Center for the Military Ethic at the US Military Academy, West Point; Distinguished Visiting Professor of Biomedical Sciences, Health Promotions, and Ethics at the Coburg University of Applied Sciences, Coburg, GER; Chair Emeritus of the Neuroethics Project of the IEEE Brain Initiative; and serves as Director of the Institute for Biodefense Research, a federally funded Washington DC think tank dedicated to addressing emerging issues at the intersection of science, technology and national defense. He previously served as Donovan Group Senior Fellow, US Special Operations Command; member of the Neuroethics, Legal, and Social Issues Advisory Panel of the Defense Advanced Research Projects Agency (DARPA); and Task Leader of the Working Group on Dual-Use of the EU-Human Brain Project. Prof. Giordano is the author of over 350 peer-reviewed publications, 9 books and 50governmental reports on science, technology, and biosecurity, and is an elected member of the European Academy of Science and Arts, a Fellow of the Royal Society of Medicine (UK), and a Fulbright Professorial Fellow. A former US Naval officer, he was winged as an aerospace physiologist, and served with the US Navy and Marine Corps.

The future of mental privacy in the neurotechnology age | Nita Farahany

Originally released December 2023._ In today’s episode, host Luisa Rodriguez speaks to Nita Farahany — professor of law and philosophy at Duke Law School — about applications of cutting-edge neurotechnology.

They cover:
• How close we are to actual mind reading.
• How hacking neural interfaces could cure depression.
• How companies might use neural data in the workplace — like tracking how productive you are, or using your emotional states against you in negotiations.
• How close we are to being able to unlock our phones by singing a song in our heads.
• How neurodata has been used for interrogations, and even criminal prosecutions.
• The possibility of linking brains to the point where you could experience exactly the same thing as another person.
• Military applications of this tech, including the possibility of one soldier controlling swarms of drones with their mind.
• And plenty more.

In this episode:
• Luisa’s intro [00:00:00]
• Applications of new neurotechnology and security and surveillance [00:04:25]
• Controlling swarms of drones [00:12:34]
• Brain-to-brain communication [00:20:18]
• Identifying targets subconsciously [00:33:08]
• Neuroweapons [00:37:11]
• Neurodata and mental privacy [00:44:53]
• Neurodata in criminal cases [00:58:30]
• Effects in the workplace [01:05:45]
• Rapid advances [01:18:03]
• Regulation and cognitive rights [01:24:04]
• Brain-computer interfaces and cognitive enhancement [01:26:24]
• The risks of getting really deep into someone’s brain [01:41:52]
• Best-case and worst-case scenarios [01:49:00]
• Current work in this space [01:51:03]
• Watching kids grow up [01:57:03]

The 80,000 Hours Podcast features unusually in-depth conversations about the world’s most pressing problems and what you can do to solve them.

Learn more, read the summary and find the full transcript on the 80,000 Hours website:

Nita Farahany on the neurotechnology already being used to convict criminals and manipulate workers

To understand cognition — and its dysfunction — neuroscientists must learn its rhythms

It could be very informative to observe the pixels on your phone under a microscope, but not if your goal is to understand what a whole video on the screen shows. Cognition is much the same kind of emergent property in the brain. It can only be understood by observing how millions of cells act in coordination, argues a trio of MIT neuroscientists. In a new article, they lay out a framework for understanding how thought arises from the coordination of neural activity driven by oscillating electric fields — also known as brain “waves” or “rhythms.”

Historically dismissed solely as byproducts of neural activity, brain rhythms are actually critical for organizing it, write Picower Professor Earl Miller and research scientists Scott Brincat and Jefferson Roy in Current Opinion in Behavioral Science. And while neuroscientists have gained tremendous knowledge from studying how individual brain cells connect and how and when they emit “spikes” to send impulses through specific circuits, there is also a need to appreciate and apply new concepts at the brain rhythm scale, which can span individual, or even multiple, brain regions.

“Spiking and anatomy are important, but there is more going on in the brain above and beyond that,” says senior author Miller, a faculty member in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences at MIT. “There’s a whole lot of functionality taking place at a higher level, especially cognition.”

Endothelial TDP-43 depletion disrupts core blood–brain barrier pathways in neurodegeneration

The study, “Endothelial TDP-43 Depletion Disrupts Core Blood-Brain Barrier Pathways in Neurodegeneration,” was published on March 14, 2025. The lead author, Omar Moustafa Fathy, an MD/Ph. D. candidate at the Center for Vascular Biology at UConn School of Medicine, conducted the research in the laboratory of senior author Dr. Patrick A. Murphy, associate professor and newly appointed interim director of the Center for Vascular Biology. The study was carried out in collaboration with Dr. Riqiang Yan, a leading expert in Alzheimer’s disease and neurodegeneration research.

This work provides a novel and significant exploration of how vascular dysfunction contributes to neurodegenerative diseases, exemplifying the powerful collaboration between the Center for Vascular Biology and the Department of Neuroscience. While clinical evidence has long suggested that blood-brain barrier (BBB) dysfunction plays a role in neurodegeneration, the specific contribution of endothelial cells remained unclear. The BBB serves as a critical protective barrier, shielding the brain from circulating factors that could cause inflammation and dysfunction. Though multiple cell types contribute to its function, endothelial cells—the inner lining of blood vessels—are its principal component.

“It is often said in the field that ‘we are only as old as our arteries’. Across diseases we are learning the importance of the endothelium. I had no doubt the same would be true in neurodegeneration, but seeing what these cells were doing was a critical first step,” says Murphy.

Omar, Murphy, and their team tackled a key challenge: endothelial cells are rare and difficult to isolate from tissues, making it even harder to analyze the molecular pathways involved in neurodegeneration.

To overcome this, they developed an innovative approach to enrich these cells from frozen tissues stored in a large NIH-sponsored biobank. They then applied inCITE-seq, a cutting-edge method that enables direct measurement of protein-level signaling responses in single cells—marking its first-ever use in human tissues.

This breakthrough led to a striking discovery: endothelial cells from three different neurodegenerative diseases—Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD)—shared fundamental similarities that set them apart from the endothelium in healthy aging. A key finding was the depletion of TDP-43, an RNA-binding protein genetically linked to ALS-FTD and commonly disrupted in AD. Until now, research has focused primarily on neurons, but this study highlights a previously unrecognized dysfunction in endothelial cells.

“It’s easy to think of blood vessels as passive pipelines, but our findings challenge that view,” says Omar. “Across multiple neurodegenerative diseases, we see strikingly similar vascular changes, suggesting that the vasculature isn’t just collateral damage—it’s actively shaping disease progression. Recognizing these commonalities opens the door to new therapeutic possibilities that target the vasculature itself.”

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Research reveals how childhood adversity shapes the brain and behavior

Early-life adversity affects more than half of the world’s children and is a significant risk factor for cognitive and mental health problems later in life. In an extensive and up-to-the-minute review of research in this domain, scholars from the University of California, Irvine illuminate the profound impacts of these adverse childhood experiences on brain development and introduce new paths for understanding and tackling them.

Their study, published in Neuron, examines the mechanisms behind the long-term consequences of childhood (). Despite extensive research spanning over seven decades, the authors point out that significant questions remain unanswered. For example, how do adults—from parents to researchers—fully comprehend what is perceived as stressful by an infant or child?

Such conceptual queries, as well as the use of cutting-edge research tools, can provide a road map, guiding experts toward developing innovative methods and providing solutions to this pressing mental health issue.

Mechanisms of chronic postsurgical pain

Central sensitization: analysis by physio meets science.

Neurophysiological Mechanism of Central Sensitization in the Spinal Cord following Surgery:

▶️ Central sensitization was first described by Woolf in 1983 (https://pubmed.ncbi.nlm.nih.gov/6656869/) as a form of long-term adaptive neuroplasticity that amplifies the transmission of nociceptive information by affecting spinal cord neurons and is believed to be a principal neurophysiological mechanism with regard to pain persistence.

▶️ Peripheral nociception can trigger a prolonged increase in the excitability of dorsal root ganglia (DRG) neurons, which transmit nociceptive signals to the spinal cord, resulting in central sensitization.

▶️ This condition involves heightened responsiveness of spinal neurons, driven by signaling molecules like adenosine triphosphate (ATP) and neurotransmitters such as glutamate (Glu) and substance P (SP).

▶️ These molecules activate specific receptors on spinal neurons, including purinergic receptor 2 (P2-R), N-methyl-D-aspartate receptor (NMDAR), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR), and neurokinin 1 receptor (NK1R).

▶️ The activation of these receptors sets off a cascade of intracellular pathways involving enzymes like calcium/calmodulin-dependent protein kinase II (CaMKII), protein kinase C (PKC), protein kinase A (PKA), mechanistic target of rapamycin (mTOR), phosphoinositide 3-kinase (PI3K), and extracellular signal-regulated kinases 1/2 (ERK1/2), all of which amplify the transmission of nociceptive signals to the brain.

Continue reading “Mechanisms of chronic postsurgical pain” | >