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Category: neuroscience – Page 92

Sleep’s dual role: How it consolidates memories while preparing the brain for new learning

Memory formation, storage, and retrieval are fundamental processes that define who we are and how we interact with the world. At the cellular level, these processes rely on specialized neurons called engram cells—neuronal populations that physically encode our experiences and allow us to recall them later. Over the past few decades, scientists have made significant progress in identifying these neuronal ensembles and understanding some aspects of memory allocation.

Although sleep is widely known to be essential for memory processing and consolidation, many of its underlying mechanisms and functions are unclear. Traditional views have largely focused on sleep as a backward-looking process that serves to strengthen past experiences, but could it simultaneously help prepare the brain for new learning?

In a recent effort to tackle this question, a research team from Japan, led by Distinguished Professor Kaoru Inokuchi from the University of Toyama, uncovered a dual role for sleep in memory processing. Their paper, which will be published in Nature Communications on April 28, 2025, explores how the brain simultaneously preserves past memories while preparing for future ones during sleep periods.

Enzymes critical for astrocytic GABA production in Alzheimer’s disease identified!

A research team has identified a previously unknown enzyme, SIRT2, that plays a key role in memory loss associated with Alzheimer’s disease (AD). The study provides critical insights into how astrocytes contribute to cognitive decline by producing excessive amounts of the inhibitory neurotransmitter GABA.

Astrocytes, once thought to only support neurons, are now known to actively influence brain function. In Alzheimer’s disease, astrocytes become reactive, meaning they change their behavior in response to the presence of amyloid-beta (Aβ) plaques, a hallmark of the disease. While astrocytes attempt to clear these plaques, this process triggers a harmful chain reaction. First, they uptake them via autophagy and degrade them by the urea cycle, as discovered in previous research. However, this breakdown results in the overproduction of GABA, which dampens brain activity and leads to memory impairment. Additionally, this pathway generates hydrogen peroxide (H2O2), a toxic byproduct that causes further neuronal death and neurodegeneration.

The research team set out to uncover which enzymes were responsible for excessive GABA production, hoping to find a way to selectively block its harmful effects without interfering with other brain functions. Using molecular analysis, microscopic imaging, and electrophysiology, the researchers identified SIRT2 and ALDH1A1 as critical enzymes involved in GABA overproduction in Alzheimer’s-affected astrocytes.

Computational mechanism underlying switching of motor actions

Author summary Humans exhibit a remarkable ability to regulate their actions in response to changing environmental demands. An essential aspect of action regulation is action inhibition that occurs when stopping unwanted or inappropriate actions. However, everyday life rarely calls for complete inhibition of responses without switching behavior to adapt to new situations. Despite extensive research to understand how the brain switches actions, the computations underlying the switching process and how it relates to the selecting and stopping processes remain elusive. Part of this challenge lies in the fact that these processes are rarely studied together, making it difficult to develop a unified theory that explains the computational aspects of the action regulation mechanism. The current study aims to delineate the computations underlying action regulation functions that involve inhibitory control, explore how these functions interrelate, and how they can be implemented within brain networks, opening new avenues for future neurophysiological investigations.

Hormone supplementation in rhesus monkeys points to potential autism treatment

For years, Florida Tech’s Catherine Talbot, an assistant professor of psychology, has worked to understand the sociality of male rhesus monkeys and how low-social monkeys can serve as a model for humans with autism. Her most recent findings show that replenishing a deficient hormone, vasopressin, helped the monkeys become more social without increasing their aggression—a discovery that could change autism treatment.

Currently, the Centers for Disease Control and Prevention reports that one in 36 children in the United States is affected by autism spectrum disorder (ASD). That’s an increase from one in 44 children reported in 2018. Two FDA-approved treatments currently exist, Talbot said, but they only address associated symptoms, not the root of ASD. The boost in both prevalence and awareness of the disorder prompts the following question: What is the cause?

Some are naturally low-social, meaning they demonstrate poor social cognitive skills, while others are highly social. Their individual variation in sociality is comparable to how human sociality varies, ranging from people we consider social butterflies to those who are not interested in social interactions, similar to some people diagnosed with ASD, Talbot said. Her goal has been to understand how variations in biology and behavior influence social cognition.

Brain’s ‘blue spot’ key to healthy aging, early Alzheimer’s detection

In a demographically diverse sample of healthy people, Cornell researchers found dramatic changes over the human lifespan in the brain’s “blue spot”—a tiny region involved in cognition and believed to be the first affected by neurodegenerative conditions including Alzheimer’s disease.

Using specialized MRI scans to measure the intensity of neuromelanin, a pigment that gives the locus coeruleus (LC) its , the research team observed an inverted U-shaped curve that peaked in later middle age before dropping off sharply, a finding that helps characterize healthy aging patterns.

Maintaining a stronger blue signal after age 60 was associated with better cognitive performance, according to the study involving 134 participants aged 19 to 86. Because of the participants’ diversity, including about 40% who were non-white, the researchers also discovered higher peaks among Black participants and women, groups known to be more susceptible to Alzheimer’s.

Nasal microbiome may help explain link between olfactory dysfunction and cognitive decline

As humans age, particularly after middle age, their brain functions, cognitive abilities and memory can deteriorate to varying degrees. Aging-related disorders marked by cognitive decline, particularly dementia, have become increasingly widespread over the past decades.

Estimates suggest that the number of individuals diagnosed with dementia could increase from 55 million in 2019 to around 139 million by 2050. Understanding the factors contributing to and devising methods to detect the first signs of dementia is thus of the utmost importance, as it could help to reliably pick up its emergence and plan therapeutic interventions accordingly.

In recent years, some studies have found a link between people’s ability to perceive and identify odors (i.e., olfactory function) and their cognitive abilities as . While the relationship between and cognitive decline is now well-documented, whether one causes the other or they are the result of similar aging-related or neurodegenerative mechanisms remains unclear.

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