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Even healthy brains become less efficient as they age, but they do so at different rates for different tasks in different people. Understanding what contributes to this decline, and the ways in which that decline varies, can provide significant insight into the function of the brain.

In a new study, researchers at The University of Texas at Dallas documented how some parts of the brain perform differently over time in response to various kinds of visual input.

A team from the Center for Vital Longevity (CVL) analyzed a phenomenon called neural dedifferentiation, in which regions of the brain that normally are specialized to perform distinct tasks become less selective in their responses to stimulus types.

The thalamus is a “Grand Central Station” for sensory information coming to our brains. Almost every sight, sound, taste and touch we perceive travels to our brain’s cortex via the thalamus. It is theorized that the thalamus plays a major role in consciousness itself. Not only does sensory information pass through the thalamus, it is also processed and transformed by the thalamus so our cortex can better understand and interpret these signals from the world around us.

One powerful type of transformation comes from interactions between excitatory neurons that carry data to the neocortex and inhibitory neurons of the thalamic reticular nucleus, or TRN, that regulate flow of that data. Although the TRN has long been recognized as important, much less has been known about what kinds of cells are in the TRN, how they are organized and how they function.

Now a paper published in the journal Nature addresses those questions. Researchers led by corresponding author Scott Cruikshank, Ph.D., and co-authors Rosa I. Martinez-Garcia, Ph.D., Bettina Voelcker, Ph.D., and Barry Connors, Ph.D., show that the somatosensory part of the TRN is divided into two functionally distinct sub-circuits. Each has its own types of genetically defined neurons that are topographically segregated, are physiologically distinct and connect reciprocally with independent thalamocortical nuclei via dynamically divergent synapses.

Goodbye depression.


Neuralink‘s mission has never quite been clear. We know it’s working on a chip designed to be surgically inserted into the human skull called a brain-computer interface (BCI), but exactly what and who it’s for remains a bit of a mystery.

As best we can tell based on what’s been revealed so far, it’s shaping up to be a terrifying hormone hijacker capable of potentially giving you forced mental orgasms or making you fall in love.

Yes.

TOKYO – Although scientists know many of the underlying symptoms which trigger Alzheimer’s disease, a cure remains elusive. Now, a new study suggests that oxytocin, a hormone best known for promoting feelings of love and wellbeing, may reverse some of the damage the degenerative illness causes.

Alzheimer’s disease is a progressive brain disease causing the continuous deterioration of mental functions. Its primary symptoms include severely impaired thinking, memory loss, and confusion.

One of the primary culprits in Alzheimer’s is a protein known as amyloid β (Aβ). Researchers say Aβ clumps together to form plaques around neurons in the brain. These plaque build-ups disrupt normal neuron function and triggers the degeneration.

Here, we discover prototypical pacemaker neurons in the ancient cnidarian Hydra and provide evidence for a direct interaction of these neurons with the commensal microbiota. We uncover a remarkable gene-expression program conservation between the Hydra pacemaker neurons and pacemaker cells in Caenorhabditis elegans and the mammalian gut. We suggest that prototypical pacemaker cells emerged as neurons using components of innate immunity to interact with the microbial environment and ion channels to generate rhythmic contractions. The communication of pacemaker neurons with the microbiota represents a mechanistic link between the gut microbiota and gut motility. Our discoveries improve the understanding of the archetypical properties of the enteric nervous systems, which are perturbed in human dysmotility-related conditions.

Pacemaker neurons exert control over neuronal circuit function by their intrinsic ability to generate rhythmic bursts of action potential. Recent work has identified rhythmic gut contractions in human, mice, and hydra to be dependent on both neurons and the resident microbiota. However, little is known about the evolutionary origin of these neurons and their interaction with microbes. In this study, we identified and functionally characterized prototypical ANO/SCN/TRPM ion channel-expressing pacemaker cells in the basal metazoan Hydra by using a combination of single-cell transcriptomics, immunochemistry, and functional experiments. Unexpectedly, these prototypical pacemaker neurons express a rich set of immune-related genes mediating their interaction with the microbial environment.

While the issue of aging and DNA methylation is an area that is well-studied, modifications of DNA to reduce or reverse aging remains an area in need of exploration. Studies in mice utilizing interventions such as caloric restriction and the drug rapamycin have reversed and/or slowed age-related DNA methylation by up to 40%. Understanding the cross-species aging based on similar DNA behaviors may open more doors to investigating therapeutics to minimize lifetime risks of age-related illnesses such as Alzheimer’s disease and cancers.


A recent study published in Cell Systems sought to debunk one of the most common myths about dogs: much to our surprise, one “dog year” does not equal seven “human years.” As described in a recent Forbes piece by Sara Tabin, the relationship between dog years and human years is not linear, but is based on a logarithmic formula. The research group, based at the University of California, San Diego (UCSD), created the formula as follows:

Age in human years = 16 ln(age in dog years) +31. (ln means “natural logarithm).