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Pancreatic insulin disruption triggers bipolar disorder-like behaviors in mice, study shows

Bipolar disorder is a psychiatric disorder characterized by alternating episodes of depression (i.e., low mood and a loss of interest in everyday activities) and mania (i.e., a state in which arousal and energy levels are abnormally high). On average, an estimated 1–2% of people worldwide are diagnosed with bipolar disorder at some point during their lives.

Bipolar disorder can be highly debilitating, particularly if left untreated. Understanding the neural and physiological processes that contribute to its emergence could thus be very valuable, as it could inform the development of new prevention and treatment strategies.

In addition to experiencing periodic changes in mood, individuals diagnosed with this disorder often exhibit some metabolic symptoms, including changes in their blood sugar levels. While some previous studies reported an association between blood sugar control mechanisms and bipolar disorder, the biological link between the two has not yet been uncovered.

Why Do We Need Sleep? Oxford Scientists Trace the Answer to Mitochondria

Sleep may serve as more than rest for the mind; it may also function as essential upkeep for the body’s energy systems. A new study from University of Oxford researchers, published in Nature, shows that the drive to sleep is caused by electrical stress building up in the tiny energy-producing structures of brain cells.

This finding provides a concrete physical explanation for the biological need for sleep and has the potential to reshape scientific thinking about sleep, aging, and neurological disorders.

Switching Off One Crucial Protein Appears to Reverse Brain Aging in Mice

A protein called ferritin light chain 1 (FTL1) may play a significant role in brain aging, a new study reveals, giving scientists a new target for understanding and potentially preventing brain deterioration and disease.

FTL1 was brought to light through a careful comparison of the hippocampus part of the brain in mice of different ages. The hippocampus is involved in memory and learning, and it is one of the regions that suffers most from age-related decline.

The study team found that FLT1 was the one protein in this region that old mice had more of and young mice had less of.

Brain cancer cells can be ‘reprogrammed’ to stop them from spreading

Scientists have found a way to stop brain cancer cells spreading by essentially ‘freezing’ a key molecule in the brain.

The finding could pave the way for a new type of treatment for , the most aggressive form of brain cancer, although extensive testing will be required before it can be trialed in patients. Glioblastoma is the most common type of brain cancer, with a five-year survival rate of just 15%.

The researchers, from the University of Cambridge, found that rely on the flexibility of (HA)—a sugar-like polymer that makes up much of the brain’s supporting structure—to latch onto receptors on the surface of cancer cells to trigger their spread throughout the brain.

Memory consolidation requires reactivation of only three neurons during sleep, research reveals

Researchers at Tsukuba University in Japan report that memories acquired while awake are stored in a more permanent form (called memory consolidation) during the REM stage of sleep, and that this process requires the reactivation of only a few specialized neurons involved in memory formation. They found that three of these neurons are crucial for memory consolidation during REM sleep.

The researchers focused on adult-born (ABNs) in the hippocampal region of the temporal lobe, which are rare neurons known to be essential for maintaining proper memory function as the loss of these cells is observed in Alzheimer’s disease. However, it has remained unclear why the loss of this small neuronal population has such devastating effects on memory.

In the Nature Communications study, specially genetically modified , in which the activity of ABNs could be monitored, were exposed to a fear experience, and the researchers examined if the activities of these ABNs during initial memory formation were reproduced during REM sleep, when dreaming is believed to occur.

Association between Coffee Consumption and Brain MRI Parameters in the Hamburg City Health Study

Despite the association of regular coffee consumption with fewer neurodegenerative diseases, it remains unclear how coffee is associated with pre-clinical brain pathologies such as lesions in the white matter, degeneration of the cortex, or alterations of the microstructural integrity. White matter hyperintensities (WMH) are hyperintense lesions on T2-weighted images and are associated with an increased risk for stroke and depression, cognitive deterioration, and gait disorders [13,14,15]. As a marker of cerebral small vessel disease (CSVD) and vascular brain damage, WMH can vary in the degree of expression, depending on the age and the presence of cardiovascular risk factors, e.g., smoking or hypertension [16,17,18]. Previous studies have reported diverging results on the association of consumed coffee with imaging markers of CSVD. They found either beneficial associations of coffee with lacunar infarcts [7], beneficial [19] or detrimental [20] associations with WMH volume, or no significant associations at all [21,22].

A recently developed and valid imaging marker of microstructural integrity is the peak width of skeletonized mean diffusivity (PSMD), calculated as the distribution of the mean diffusivity (MD) between the 5th and 95th percentile in the white matter skeleton [23]. Only one study analyzed the association of coffee consumption with microstructural integrity, as quantified by fractional anisotropy, with a higher coffee consumption being associated with higher integrity of the white matter microstructure [24].

Damage to the brain structure is not restricted to white matter, but also extents to the cortex, e.g., in the form of atrophy. Except for one study focusing on the quantification of cortical thickness in regions susceptible for Alzheimer’s Disease [22], the link between coffee consumption and cortical thickness was only indirectly examined by measuring total brain volume or grey matter volume, with incongruent results between studies [7, 21,25,26]. This study aimed at investigating whether coffee consumption is associated with multiple brain MRI markers of vascular brain damage and neurodegeneration, including WMH, PSMD, and cortical thickness in a large, population-based cohort.

Rare seasonal brain shrinkage in shrews is driven by water loss

Water cure: The study found that common shrews shrink their brains in winter not by losing cells, but by losing water.

Brain scans: The team used MRI scanning, the same technology used in hospitals, to peer inside the brains of live shrews across seasons.

What humans can learn: Brain shrinkage in humans is typically a sign of disease, like Alzheimer’s. But shrews can shrink their brain without compromising function or causing damage. Shrews could become a model system for exploring potential pathways for medica treatment of human brain disease.


Knowing how shrews loose brain volume over winter is the first step to understanding how they reverse this loss and regrow healthy brains in summer.

Brain.

Your Mother’s Germs May Have Influenced Your Brain’s Development

Our bodies are colonized by a teeming, ever-changing mass of microbes that help power countless biological processes. Now, a new study has identified how these microorganisms get to work shaping the brain before birth.

Researchers at Georgia State University studied newborn mice specifically bred in a germ-free environment to prevent any microbe colonization. Some of these mice were immediately placed with mothers with normal microbiota, which leads to microbes being transferred rapidly.

That gave the study authors a way to pinpoint just how early microbes begin influencing the developing brain. Their focus was on the paraventricular nucleus (PVN), a region of the hypothalamus tied to stress and social behavior, already known to be partly influenced by microbe activity in mice later in life.

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