Toggle light / dark theme

A new neuroimaging study showed that people suffering from posttraumatic stress disorder (PTSD) exhibited increased activation in the amygdala region of the brain when shown surprised and neutral facial expressions. The same phenomenon was observed in identical twins of these individuals who did not suffer from PTSD.

The study, which was published in the Journal of Psychiatric Research, sheds new light on the neural mechanisms underlying the development of PTSD.

PTSD is a condition that develops in approximately 20% of individuals exposed to psychological trauma in their lifetime. It is defined by wide clusters of symptoms that include intrusive memories, negative alterations in mood, heightened levels of arousal, and other symptoms. Currently, there are many treatment options available for PTSD; however, for some patients, the treatments offered do not provide clinical relief.

Through the issue of mental representation addressed in the previous article, it is possible to get a first idea about the theoretical discontinuity between traditional cognitive science and more recent approaches gathered under the umbrella of so-called 4E Cognition. In fact, in many cases those latter reflect — directly or in a collateral way — the attempt to overcome the problem of representation in human cognition, even thought, as we’re going to say, this doesn’t entail a unite consensus at all.

4E Cognition has not to be seen as a specific and well-defined theoretical system, rather, it is a term referring to all those works (hypothesis, theories, experiments, etc.) which deviate from the traditional representational-computational model of cognition (see part 1), taking a dynamic and enactive approach, namely, conceiving cognition as embodied, embedded, enactive and extended (that’s why 4E). In a nutshell, mental states and cognitive processes would be: embodied when they are partly constituted by bodily processes; embedded when there is an essential causal dependence between such states and processes and the environment; enacted when the actions of the subject can partly constitute these states and processes; and extended when objects or processes in the environment can partly constitute those states and processes [4].

Here you can find a quick conversational introduction to 4E cognition made by professor Shaun Gallagher:

Bryan Johnson releases his rejuvenation protocol:


Blueprint is a public science experiment to determine whether it’s possible to stay the same biological age. This requires slowing down aging processes as much as possible and then reversing the aging that has happened. Currently my speed of aging is .76 (DunedinPACE). That means for every 365 days each year, I age 277 days. My goal is to remain the same age biologically for every 365 days that pass.

I openly share (for free!) my diet, exercise and other protocols so that others can benefit and try to improve upon what I’m doing. I also openly share my health data as data is better than human opinion at guiding decision making. You can find everything here: https://blueprint.bryanjohnson.co/

This video is a whirlwind tour of what my daily life looks like as my team and I are on this adventure.

On the surface, Blueprint may seem like something about health, wellness and aging. To me, it’s a philosophy.

Twelve-hour (12 h) ultradian rhythms are a well-known phenomenon in coastal marine organisms. While 12 h cycles are observed in human behavior and physiology, no study has measured 12 h rhythms in the human brain. Here, we identify 12 h rhythms in transcripts that either peak at sleep/wake transitions (approximately 9 AM/PM) or static times (approximately 3 PM/AM) in the dorsolateral prefrontal cortex, a region involved in cognition. Subjects with schizophrenia (SZ) lose 12 h rhythms in genes associated with the unfolded protein response and neuronal structural maintenance. Moreover, genes involved in mitochondrial function and protein translation, which normally peak at sleep/wake transitions, peak instead at static times in SZ, suggesting suboptimal timing of these essential processes.

You can grasp a hand. You can also grasp a concept. One is literal. One is metaphorical. Our brains know the difference, but would we be able to understand the latter without the former?

Previous studies have suggested that our understanding of metaphors may be rooted in our bodily experience. Some functional MRI, o fMRI, brain imaging studies have indicated, for example, that when you hear a metaphor such as “she had a rough day,” regions of the brain associated with tactile experience are activated. If you hear, “he’s so sweet,” areas associated with taste are activated. And when you hear action verbs used in a metaphorical context, like “grasp a concept,” regions involved in motor perception and planning are activated.

A study by University of Arizona researcher Vicky Lai, published in the journal Brain Research, builds on this research by looking at when, exactly, different regions of the brain are activated in metaphor comprehension and what that tells us about the way we understand .

More than one-third of UK health experts are not aware of Charles Bonnet syndrome — CBS — a condition which can cause vivid, and sometimes frightening, hallucinations.

A poll of 1,100 health experts — including GPs, doctors and optometrists — found 37 per cent were not aware of CBS.

The condition is not caused by mental health problems or dementia. It is purely due to a loss of sight — 60 per cent or more — which reduces or stops the regular messages from the eye to the brain.

The human brain is a complex system exhibiting multi-scale spatiotemporal organization. In this talk, I will provide an overview of my lab’s work on large-scale functional network organization across different timescales. First, I will present a biophysically plausible model of second-level fluctuation in the brain’s functional connectivity patterns. I will then discuss how minute-level task-state changes can predict behavioral traits. This is followed by exploring how brain dynamics can vary over the course of a day. Finally, I will discuss our work on estimating individual-level network markers that are stable across weeks and months.

This video is part of the SNAC seminar series organized by Mac Shine, Joe Lizier, and Ben Fulcher (The University of Sydney).

We spoke with Dr Morgan Levine 2 years ago concerning the remarkable results that she and a team that included Dr David Sinclair had in restoring vision in mice. In that experiment, published in the journal Nature, older mice had tighter optic nerves crushed causing blindness. Then, using a combination of 3 of the 4 Yamanaka cellular programing factors, they were able to restore the mice’s vision by signally the underlying DNA, rebuilding what had been thought to be permanently damaged cells. This was a remarkable result, as it was restoring a damaged organ, essentially a part of the brain, to its original healthy state. When I spoke to Dr Levine about the next step in her research, she mentioned it may be a more complex organ, such as a mouse liver.

But they went further. In the January issue of Cell, Sinclair published results of their ability to age an entire mouse. That is, to signal the epigenome to cause the underlying mouse DNA to behave as if it were much older. They were also able to do the reverse: to take an older mouse and, by signaling the epigenome, bring its cells and organs to the state of a younger mouse. This is a truly remarkable achievement, and it seems to prove Sinclair’s theory that all of our cells have within them a pristine copy of their DNA, and that aging and the disease associated with aging are the result of miscues from the epigenome. If these miscues can be corrected then the cell can be restored, not to a blank stem cell but to its original condition.

Summary: The Mini2P microscope can be used to record brain activity in live, freely moving mice.

Source: NTNU

The Chan Zuckerberg Initiative, established by Mark Zuckerberg and his wife, Dr. Priscilla Chan, has awarded a grant of between NOK 5–6 million (approx $500 000-$60000 USD) to the Norwegian University of Science and Technology’s Kavli Institute for Systems Neuroscience.