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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.”

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.”

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.

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.

Key Takeaways A study found that some organs age faster than a person’s actual ageFaster organ aging is linked to diseases like cancer, dementia and heart diseaseA blood test could help detect early signs of organ aging.

MONDAY, March 17, 2025 (HealthDay News) — Your organs might be aging faster than you are — and that could increase your risk for serious diseases, including cancer, heart disease and dementia.

A new study probing quantum phenomena in neurons as they transmit messages in the brain could provide fresh insight into how our brains function.

In this project, described in the Computational and Structural Biotechnology Journal, theoretical physicist Partha Ghose from the Tagore Centre for Natural Sciences and Philosophy in India, together with theoretical neuroscientist Dimitris Pinotsis from City St George’s, University of London and the MillerLab of MIT, proved that established equations describing the classical physics of brain responses are mathematically equivalent to equations describing quantum mechanics. Ghose and Pinotsis then derived a Schrödinger-like equation specifically for neurons.

Our brains process information via a vast network containing many millions of neurons, which can each send and receive chemical and electrical signals. Information is transmitted by nerve impulses that pass from one neuron to the next, thanks to a flow of ions across the neuron’s cell membrane. This results in an experimentally detectable change in electrical potential difference across the membrane known as the “action potential” or “spike”

The activity of microglia is fundamental for the regulation of numerous physiological processes including brain development, synaptic plasticity, and neurogenesis, and its deviation from homeostasis can lead to pathological conditions, including numerous neurodegenerative disorders. Carnosine is a naturally occurring molecule with well-characterized antioxidant and anti-inflammatory activities, able to modulate the response and polarization of immune cells and ameliorate their cellular energy metabolism. The better understanding of microglia characteristics under basal physiological conditions, as well as the possible modulation of the mechanisms related to its response to environmental challenges and/or pro-inflammatory/pro-oxidant stimuli, are of utmost importance for the development of therapeutic strategies.

In the following paper, the authors aimed to compare the social cognition profiles of individuals with cerebellar neurodegenerative disorders, autism, bipolar disorder type 2, or healthy subjects using a battery of social tests requiring different degrees of prediction processing.

📝 — Olivito, et al.

Full text is available 👇


Social prediction is a key feature of social cognition (SC), a function in which the modulating role of the cerebellum is recognized. Accordingly, cerebellar alterations are reported in cerebellar pathologies, neurodevelopmental disorders, and psychiatric conditions that show SC deficits. Nevertheless, to date, no study has directly compared populations representative of these three conditions with respect to SC and cerebellar alterations. Therefore, the present exploratory study aimed to compare the SC profiles of individuals with cerebellar neurodegenerative disorders (CB), autism (ASD), bipolar disorder type 2 (BD2), or healthy subjects (HS) using a battery of social tests requiring different degrees of prediction processing. The patterns of cerebellar gray matter (GM) alterations were compared among the groups using voxel-based morphometry.

Each year, according to the National Institutes of Health (NIH), millions of people in the U.S. are affected by spinal cord and traumatic brain injuries, along with neuro-developmental and degenerative diseases such as ADHD, autism, cerebral palsy, Alzheimer’s disease, multiple sclerosis, epilepsy and Parkinson’s disease.

Assistant Professor Pabitra Sahoo, of Rutgers University-Newark’s Department of Biological Sciences, has made it his life’s work to understand how our neurological system becomes damaged by these injuries and conditions, and when and how neurons in our central and peripheral nervous systems regenerate and heal.

Recently, Sahoo and his RU-N research team made a breakthrough, using a peptide to help nerve cells in both the peripheral and central nervous systems regenerate. They published their findings in Proceedings of the National Academy of Sciences.

Around 15 percent of the world’s population suffers from tinnitus, a condition which causes someone to hear a sound (such as ringing or buzzing) without any external source. It’s often associated with hearing loss.

Not only can the condition be annoying for sufferers, it can also have a serious effect on mental health, often causing stress or depression. This is especially the case for patients suffering from tinnitus over months or years.

There’s currently no cure for tinnitus. So finding a way to better manage or treat it could help many millions of people worldwide.