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We named him Squirt—not because he was the smallest of the 16 cuttlefish in the pool, but because anyone with the audacity to scoop him into a separate tank to study him was likely to get soaked. Squirt had notoriously accurate aim.

As a comparative psychologist, I’m used to assaults from my experimental subjects. I’ve been stung by bees, pinched by crayfish and battered by indignant pigeons. But, somehow, with Squirt it felt different. As he eyed us with his W-shaped pupils, he seemed clearly to be plotting against us.

Of course, I’m being anthropomorphic. Science does not yet have the tools to confirm whether cuttlefish have emotional states, or whether they are capable of conscious experience, much less sinister plots. But there’s undeniably something special about cephalopods—the class of ocean-dwelling invertebrates that includes cuttlefish, squid and octopus.

It’s estimated that anywhere from three to seven percent of school-age children may have dyslexia, a neurodevelopmental issue that affects reading, spelling, and writing. There are different ideas about why dyslexia occurs, although they relate to dysfunction in brain networks, and are likely due to multiple causes in affected individuals; the disorder may not have a singular underlying cause. Neuroimaging studies of dyslexic individuals have produced inconsistent results.

Since dyslexia has a heritable, and therefore, genetic component, scientists wanted to know more about how genetics and brain mapping could reveal more about the pathology of dyslexia. A new study has shown that carriers of genetic variants that increase the risk of dyslexia also have changes in brain structure, which occur in areas that are related to language, motor coordination, and vision. The findings have been reported in Science Advances.

The breakthrough marks a promising target for drug therapies that slow, possibly reverse, the disease’s development

NEW YORK, NY, December 23, 2024 — Researchers with the CUNY ASRC have unveiled a critical mechanism that links cellular stress in the brain to the progression of Alzheimer’s disease (AD). The study, published in the journal Neuron, highlights microglia, the brain’s primary immune cells, as central players in both the protective and harmful responses associated with the disease.

Microglia, often dubbed the brain’s first responders, are now recognized as a significant causal cell type in Alzheimer’s pathology. However, these cells play a double-edged role: some protect brain health, while others worsen neurodegeneration. Understanding the functional differences between these microglial populations has been a research focus for Pinar Ayata, the study’s principal investigator and a professor with the CUNY ASRC Neuroscience Initiative and the CUNY Graduate Center’s Biology and Biochemistry programs.

A new study from Northwestern Medicine reports that, much like a conductor harmonizes various instruments in an orchestra to create a symphony, breathing synchronizes hippocampal brain waves to enhance memory during sleep.

This is the first time breathing rhythms during sleep have been linked to these hippocampal brain waves — called slow waves, spindles, and ripples — in humans. Scientists knew these waves were linked to memory but their underlying driver was unknown.

“To strengthen memories, three special neural oscillations emerge and synchronize in the hippocampus during sleep, but they were thought to come and go at random times,” said senior study author Christina Zelano, professor of neurology at Northwestern University.

Exercise improves cognitive performance for over 24 hours, especially when paired with good sleep. A study of older adults links physical activity and deep sleep to better memory, highlighting the importance of an active lifestyle for brain health.

Exercise provides a short-term boost to brain function that can last throughout the next day, according to a new study by researchers at University College London (UCL).

Earlier research conducted in controlled laboratory settings revealed that cognitive performance improves in the hours following exercise. However, the duration of these benefits remained unclear.

Researchers at the California Institute of Technology have unveiled a startling revelation about the human mind: our thoughts move at a mere 10 bits per second, a rate that pales in comparison to the staggering billion bits per second at which our sensory systems gather environmental data. This discovery, published in the journal Neuron, is challenging long-held assumptions about human cognition.

The research, conducted in the laboratory of Markus Meister, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences at Caltech, and spearheaded by graduate student Jieyu Zheng, applied information theory techniques on an extensive collection of scientific literature. By analyzing human behaviors such as reading, writing, video gaming, and Rubik’s Cube solving, the team calculated the 10 bits per second figure – a rate that Meister describes as “extremely low.”

To put this in perspective, a typical Wi-Fi connection processes about 50 million bits per second, making our thought processes seem glacial by comparison. This stark contrast raises a paradox that Meister and his team are eager to explore further: “What is the brain doing to filter all of this information?”

Discovery draws surprising parallels between low-level organisms and sophisticated neurons; lays the groundwork for memory-capable biological systems.

Biologists studying collectives of bacteria, or “biofilms,” have discovered that these so-called simple organisms feature a robust capacity for memory.

Working in the laboratory of University of California San Diego Professor Gürol Süel, Chih-Yu Yang, Maja Bialecka-Fornal and their colleagues found that bacterial cells stimulated with light remembered the exposure hours after the initial stimulus. The researchers were able to manipulate the process so that memory patterns emerged.

The evidence presented by Boldrini et al2 was considered resilient and convincing because the authors ensured that the samples were taken from healthy individuals using more biological parameters, such as angiogenesis and change in volume of DG, for a suitable comparison. They also employed unbiased stereology, which is the gold standard for counting number of neurons.2

The contrary results presented by the Sorrels study and Boldrini study highlight the existing ambiguity regarding the concept of neurogenesis in adult humans. Both studies employed reasonably similar immunohistological methods and included many of the same neurogenesis markers, yet contrasting results were observed. The study by Boldrini et al examined samples from humans aged 14 to 79 years, finding more than a thousand cells in each part of the DG, which was in stark contrast to what was observed by Sorrells et al, who found very few cells in the neurogenic niche of subjects in the same age range. Even if we consider that some discrepancies in numbers might arise due to the difference in counting methods (or subjective reasons), such marked and obvious disparity is perplexing. Sorrels et al justified their findings, noting the limitation that relying solely on the presence of markers might cause glial lineage cells to be identified as neuronal lineage cells. However, the authors stated that they used additional methods for confirmation, including transmission electron microscopy (TEM)-immunogold and in-situ hybridization. The relative paucity of any type of progenitor or immature cells, including glia in the neurogenic niche of DG in their study, remains unexplained.

Kempermann et al7 expressed skepticism regarding the negative findings of Sorrells et al, naming the postmortem interval, the lack of known status regarding neuropsychiatric disease or chronic ailment, and using patients with epilepsy as key factors of concern.7 Kempermann et al argued that, in severe epilepsy, destruction of the neurogenic niche is an explicit possibility, and that, in some cases, epilepsy could be the reason for the lack of neurogenesis.7 Additionally, Kempermann et al also criticized the use of 10% formalin in some of the samples due its potential to mask the expression of proteins.7 However, Sorrells et al clearly mentioned that they performed appropriate antigen retrieval for the selected sections.1 Kempermann et al7 suggested that dependence on the protein markers to denote neurogenesis could be an erroneous approach and that some of the markers, such as DCX, are known for fast degradation. Additionally, the presence of DCX-negative immature neurons and high inter-individual variation in expression of DCX in humans, which was also reflected in the data presented by Boldrini et al, are not unusual.7 The use of fluorescence markers also was presented as a caveat by Kempermann et al7 because it is prone to fade away and might give rise to false negative impression.