Researchers have uncovered a mechanism that may trigger ALS’s earliest stages, identifying proteins that mislocalize, causing neuron degeneration. By targeting the RNA-binding protein SmD1, scientists were able to prevent key ALS proteins from leaving their protective cellular zones, preserving neuron function. The findings may lead to ALS therapies capable of halting progression before significant neurodegeneration occurs, offering potential new strategies against the disease.
Researchers discovered alcohol use disorder (AUD) and Alzheimer's disease (AD) exhibit similar patterns of gene dysregulation, hinting that alcohol consumption may hasten Alzheimer’s progression. By analyzing gene expression across individual brain cells, the team found shared disruptions in inflammation, cell signaling, and blood vessel functions in both disorders.
Many animals, including humans, have developed a taste for alcohol in some form, but excessive consumption often leads to adverse health effects. One exception is the Oriental hornet. According to a new paper published in the Proceedings of the National Academy of Sciences, these hornets can guzzle seemingly unlimited amounts of ethanol regularly and at very high concentrations with no ill effects—not even intoxication. They pretty much drank honeybees used in the same experiments under the table.
“To the best of our knowledge, Oriental hornets are the only animal in nature adapted to consuming alcohol as a metabolic fuel," said co-author Eran Levin of Tel Aviv University. "They show no signs of intoxication or illness, even after chronically consuming huge amounts of alcohol, and they eliminate it from their bodies very quickly."
Per Levin et al., there's a "drunken monkey" theory that predicts that certain animals well-adapted to low concentrations of ethanol in their diets nonetheless have adverse reactions at higher concentrations. Studies have shown that tree shrews, for example, can handle concentrations of up to 3.8 percent, but in laboratory conditions, when they consumed ethanol in concentrations of 10 percent or higher, they were prone to liver damage.
Zettabytes—that’s 1021 bytes—of data are currently generated every year. All of those cat videos have to be stored somewhere, and DNA is a great storage medium; it has amazing data density and is stable over millennia.
To date, people have encoded information into DNA the same way nature has, by linking the four nucleotide bases comprising DNA—A, T, C, and G—into a particular genetic sequence. Making these sequences is time-consuming and expensive, though, and the longer your sequence, the higher chance there is that errors will creep in.
But DNA has an added layer of information encoded on top of the nucleotide sequence, known as epigenetics. These are chemical modifications to the nucleotides, specifically altering a C when it comes before a G. In cells, these modifications function kind of like stage directions; they can tell the cell when to use a particular DNA sequence without altering the “text” of the sequence itself. A new paper in Nature describes using epigenetics to store information in DNA without needing to synthesize new DNA sequences every time.
Researchers have identified a crucial biochemical mechanism that could allow Huntington’s disease to be studied before symptoms appear, offering hope for early intervention. The team found that disrupted dopamine regulation in specific neurons, related to TrkB neurotrophin receptor signaling, may trigger Huntington’s onset. By targeting an enzyme called GSTO2, researchers prevented motor symptoms in a mouse model, suggesting this protein's role in the disease's progression.
Childhood attention issues, coupled with genetic predispositions, increase the likelihood of experiencing psychotic-like symptoms in adolescence. By analyzing data from 10,000 youths, researchers discovered that variability in attention spans partially explains how genetic risk factors translate into psychotic-like symptoms.
Yamanaka factors can reverse aging in brain neurons, improving synaptic connections, metabolism, and protecting against neurodegenerative diseases like Alzheimer's. Researchers introduced the Yamanaka factors into neurons of adult mice, finding that this process rejuvenated the cells without negative side effects, even enhancing motor and social behaviors.
A new study has developed a breakthrough biomedical tool that can deliver genetic material to edit faulty genes in fetal brain cells. Tested in mice, this technology offers the potential to stop the progression of neurodevelopmental conditions, like Angelman and Rett syndromes, before birth.
Researchers have created "mini-brains" using stem cells from patients with a rare form of autism, allowing them to study brain development in detail. These organoids revealed how a genetic mutation in MEF2C disrupts the balance between excitatory and inhibitory neurons, leading to autism.
Cannabis use in adolescents may lead to thinning of the cerebral cortex, a key brain region for cognitive function. Researchers found that THC, the active ingredient in cannabis, causes the shrinking of dendrites, which are crucial for neuron communication.
Colossal, the company founded to try to restore the mammoth to the Arctic tundra, has also decided to tackle a number of other species that have gone extinct relatively recently: the dodo and the thylacine. Because of significant differences in biology, not the least of which is the generation time of Proboscideans, these other efforts may reach many critical milestones well in advance of the work on mammoths.
Late last week, Colossal released a progress report on the work involved in resurrecting the thylacine, also known as the Tasmanian tiger, which went extinct when the last known survivor died in a zoo in 1936. Marsupial biology has some features that may make de-extinction somewhat easier, but we have far less sophisticated ways of manipulating it compared to the technology we've developed for working with the stem cells and reproduction of placental mammals. But, based on these new announcements, the technology available for working with marsupials is expanding rapidly.
Cane toad resistance
Colossal has branched out from its original de-extinction mission to include efforts to keep species from ever needing its services. In the case of marsupial predators, the de-extinction effort is incorporating work that will benefit existing marsupial predators: generating resistance to the toxins found on the cane toad, an invasive species that has spread widely across Australia.
A recent study highlights a novel gene, lipin1, that regulates axon regeneration in the central nervous system, offering new hope for treating spinal cord injuries. The research shows that inhibiting lipin1 enhances lipid metabolism in neurons, activating crucial pathways like mTOR and STAT3 that promote nerve regeneration.
Researchers developed an AI algorithm, ARC-SV, to detect complex structural variants in the human genome that previous methods missed. Analyzing over 4,000 genomes, researchers discovered thousands of complex variants, many affecting brain-related genes and linked to schizophrenia and bipolar disorder.
A new study reveals that ancient viral DNA embedded in the human genome is associated with genetic risk for amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS). Researchers found specific human endogenous retroviruses (HERVs) that influence susceptibility to these neurodegenerative diseases.
A large-scale study identified 254 genetic variants that shape the volume of key brain regions responsible for memory, motor control, and behavior. Researchers analyzed DNA and brain scans from nearly 75,000 people, uncovering links between these variants and conditions like ADHD and Parkinson’s disease.
New research suggests that the Y chromosome may be responsible for the higher prevalence of autism in males, shifting focus away from protective factors on the X chromosome. Analyzing genetic data, researchers found that individuals with an additional Y chromosome were twice as likely to have an autism diagnosis, while an extra X chromosome had no effect on autism risk.
Researchers have discovered that the enzyme ATP-citrate lyase (ACLY) plays a critical role in driving the inflammatory process linked to aging, known as the senescence-associated secretory phenotype (SASP). The study shows that blocking ACLY can reduce the expression of inflammation-related genes in aging cells, opening the door for potential therapies to combat age-related diseases like dementia and atherosclerosis.
A study has found that traumatic brain injury (TBI) increases the risk of Alzheimer’s disease by disrupting protein clearance, leading to the accumulation of toxic tau proteins in the brain. Researchers discovered that TBI downregulates BAG3, a protein crucial for clearing damaged proteins, which contributes to Alzheimer's-related tau buildup.
Frequent use of high-potency cannabis leaves unique molecular marks on DNA, particularly affecting genes related to energy and immune function. Researchers found that DNA methylation—an epigenetic modification—differed between frequent cannabis users who had experienced psychosis and those who had not, suggesting a possible genetic link to psychosis risk.
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Researchers have uncovered a mechanism that may trigger ALS’s earliest stages, identifying proteins that mislocalize, causing neuron degeneration. By targeting the RNA-binding protein SmD1, scientists were able to prevent key ALS proteins from leaving their protective cellular zones, preserving neuron function. The findings may lead to ALS therapies capable of halting progression before significant neurodegeneration occurs, offering potential new strategies against the disease. 
