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Scientists at the Okinawa Institute of Science and Technology (OIST), the National Institute of Information and Communications Technology, and the University of Tokyo have found a mathematical connection between spatial navigation and language processing, creating a model called “Disentangled Successor Information” (DSI).

This model generates patterns that closely resemble the activity of actual brain cells involved in both spatial awareness (place cells and grid cells) and concept recognition (concept cells).

The DSI model shows that the hippocampus and entorhinal cortex— previously known primarily for —likely use comparable computational processes to handle both physical spaces and meaningful ideas or words. Using this shared framework, both types of information can be processed through similar mathematical computations, which could be achieved in the brain by partial activation of specific groups of neurons.

Mind Control: Past and Future https://www.hks.harvard.edu/sites/default/files/2025-01/24_Meier_02.pdf


On Jan. 28, 2024, Noland Arbaugh became the first person to receive a brain chip implant from Neuralink, the neurotechnology company owned by Elon Musk. The implant seemed to work: Arbaugh, who is paralyzed, learned to control a computer mouse with his mind and even to play online chess.

The device is part of a class of therapeutics, (BCIs), that show promise for helping people with disabilities control prosthetic limbs, operate a computer, or translate their thoughts directly into speech. Current use of the technology is limited, but with millions of global cases of spinal cord injuries, strokes, and other conditions, some estimates put the market for BCIs at around $400 billion in the U.S. alone.

A new discussion paper from the Carr Center for Human Rights welcomes the potential benefits but offers a note of caution drawn from the past, detailing unsettling parallels between an era of new therapies and one of America’s darkest chapters: experiments into psychological manipulation and mind control.

For decades, scientists have focused on amyloid plaques—abnormal clumps of misfolded proteins that accumulate between neurons—as a therapeutic target for Alzheimer’s disease. But anti-amyloid therapies haven’t made strong headway in treating the devastating condition.

Now, researchers at Yale School of Medicine (YSM) are zeroing in on a byproduct of these plaques, called axonal spheroids, and exploring how to reverse their growth. They published their findings March 10 in Nature Aging.

Axonal spheroids are bubble-like structures on axons—the part of the neuron that sends messages through electrical impulses—that form due to swelling induced by amyloid plaques. Previous research at YSM has shown that as these spheroids grow, they block electricity conduction in the axons, which can hinder the ability to communicate with other neurons.

Summary: New research highlights a critical link between antibodies produced against Epstein-Barr virus (EBV) and the development of multiple sclerosis (MS). Scientists discovered that these viral antibodies mistakenly target a protein called GlialCAM in the brain, triggering autoimmune responses associated with MS.

The study also revealed how combinations of genetic risk factors and elevated viral antibodies further increase the risk of developing MS. These insights may pave the way for improved diagnostics and targeted therapies, enhancing our understanding of the genetic and immunological interplay underlying this debilitating disease.

Is an in-depth investigation featuring world renowned philosophers and scientists into the most profound philosophical debate of all time: Do we have free will?

Featuring: Sean Carroll, Daniel Dennett, Jerry Coyne, Dan Barker, Heather Berlin, Gregg Caruso, Massimo Pigliucci, Alex O’Conner, Coleman Hughes, Edwin Locke, Robert Kane, Rick Messing, Derk Pereboom, Richard Carrier, Trick Slattery, Dustin Kreuger, Steven Sharper, Donia Abouelatta.

Chapters.

Intro: — 0:00
Chapter 1: What is Free Will? — 4:19
Chapter 2: The Problem of Free Will — 15:29
Interlude: 22:33
Chapter 3: Libertarian Free Will — 23:16
Chapter 4: Compatibilism — 34:47
Chapter 5: Free Will Skepticism — 45:13
Interlude: The 3 Positions of Free Will — 55:45
Chapter 6: The Great Debate — 57:28
Chapter 7: Neuroscience — 1:07:28
Chapter 7: The Interaction Problem — 1:18:37
Chapter 8: Physics — 1:20:10
Chapter 8: Reduction & Emergence — 1:22:14
Chapter 9: Can We Have Determinism and Free Will? — 1:28:57
Chapter 10: Free Will and the Law — 1:45:57
Chapter 11: Should We Stop Using the Term Free Will? — 1:56:37
Outro: 2:00:38

Although it’s not the first time this was hypothesized, this study is the first time researchers looked at the presence of gingipains within the brains of diseased patients. Even more, the patients themselves were never even diagnosed with Alzheimer’s.

“Our identification of gingipain antigens in the brains of individuals with AD and also with AD pathology but no diagnosis of dementia argues that brain infection with P. gingivalis is not a result of poor dental care following the onset of dementia or a consequence of late-stage disease, but is an early event that can explain the pathology found in middle-aged individuals before cognitive decline,” the authors explained.

While this isn’t a one-size-fits-all answer to what causes Alzheimer’s, it’s a step in the right direction to finding the reasoning behind this life-altering disease.

National Institutes of Health researchers have mapped how individual neurons in the primary somatosensory cortex receive brain-wide presynaptic inputs that encode behavioral states, refining our understanding of cortical activity.

Neurons in the primary somatosensory cortex process different types of sensory information and exhibit distinct activity patterns, yet the cause of these differences has remained unclear. Previous research emphasized the role of motor cortical regions in movement-related processing, but also recognized that the thalamus plays a role beyond sensory relay.

Using high-resolution single-cell mapping to trace , the team revealed that thalamic input is the primary driver for movement-correlated neurons, while motor cortical input plays a smaller role.

A recent study by the Hector Institute for Translational Brain Research (HITBR) at the Central Institute of Mental Health (CIMH) in Mannheim provides the first detailed cellular insights into how psilocin, the active ingredient in magic mushrooms, promotes the growth and networking of human nerve cells.

These findings complement clinical studies on the treatment of mental disorders and could contribute to a better understanding of the neurobiological mechanisms behind the therapeutic effect of psilocybin.

Psilocybin is the well-known in so-called magic mushrooms, which is converted in the body to psilocin—the compound that ultimately unleashes the psychoactive effect. The Mannheim research team worked directly with psilocin to investigate the neurobiological effects.