Researchers found that neural stem cells can adapt to stressful environments by producing more neurons when conditions become favorable. The study suggests a novel form of brain plasticity and potential treatment for neurodegenerative diseases.
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Researchers found that new neurons in adult monkeys take more than six months to mature, which challenges the notion that this process is related to the effectiveness of antidepressant medications. This finding suggests that the human brain may experience even longer maturation periods due to its larger size.
A team at the University of Pittsburgh has created living models of brain cells that can transmit electrical impulses and remain active for extended periods, providing a new view on memory formation. This work reveals the intricate connections between neurons and offers insights into the cellular mechanisms underlying memory creation.
Researchers have identified a protective molecule in the brain that can rescue damaged cells and prevent further damage. By artificially increasing levels of this compound, KCC2, scientists hope to develop new treatments for conditions like stroke, epilepsy, and Alzheimer's.
A study from Cold Spring Harbor Laboratory suggests that adult stem cells in the brain are 'disposable' and lose their ability to produce neurons with age, leading to a decline in new neuron production. This decline may contribute to age-related cognitive decline.
Researchers at Scripps Research Institute identified a change in calcium influx into specific brain neurons that is fundamental to long-term memory. This increase, known as a memory trace, is observed in normal fruit flies but absent in mutants with impaired long-term memory.
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A study by NIH-funded researchers has found that boosting adult neurogenesis in the hippocampus improves pattern recognition abilities, similar to those seen in younger brains. However, combining this with exercise was necessary for antidepressant-like effects to emerge.
Researchers at Columbia University have developed a new way to stimulate neuron production in the adult mouse brain, improving cognitive functions. The study suggests that stimulating neurogenesis may contribute to treatment of anxiety disorders, including PTSD and panic disorder, by enhancing pattern separation.
Researchers at UT Southwestern Medical Center found that neural stem cells in the brain's memory area become activated after injury and remodel the area with newly generated nerve cells, but this process may be limited by a finite pool of stem cells.
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Researchers at Northwestern University have successfully reprogrammed human embryonic stem cells to produce critical neurons lost in Alzheimer's disease. This breakthrough allows for rapid drug testing and the possibility of transplanting these new neurons into people with Alzheimer's, which could help preserve memory function.
Researchers at Northwestern University have made a groundbreaking discovery in the field of neuroscience, finding that axons can transmit signals to the cell body and even communicate with each other. This challenges conventional wisdom on how neurons operate, revealing a new layer of complexity in neural communication.
Researchers find that weak electrical fields in brain help neurons fire together, even if they're not physically connected. The findings suggest an additional form of neural communication through extracellular space.
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Researchers at UCLA have made a groundbreaking discovery about neuronal gap junctions, which could lead to new treatments for anxiety disorders like PTSD. The study found that blocking these gap junctions can disrupt critical rhythms in the brain region most involved in cognition, preventing fear memories from forming.
USF researchers discovered that human umbilical cord blood cells (HUCB) promote the growth and differentiation of hippocampal neurons in both young and old laboratory animals. HUCBs have been found to enhance survival, maturation, and arborization of key brain cells, potentially benefiting treating brain injury and degenerative disease...
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Research by University of California, Berkeley psychologists found that chronic jet lag causes persistent changes in the brain's hippocampus, leading to memory and learning problems. The study, which used female Syrian hamsters as subjects, showed that even after recovery from jet lag, the brain continued to experience deficits.
A novel form of splicing in the cytoplasm of nerve cells dictates a special form of a potassium channel protein in the outer membrane, essential for coordinating electrical firing of nerve cells. This discovery highlights the importance of introns in regulating protein diversity and has implications for brain diseases such as epilepsy.
Gladstone scientists discovered a process by which Alzheimer's disease spreads through the brain, starting in vulnerable regions like the entorhinal cortex. The study suggests targeting this region could be an effective therapeutic approach.
Researchers at Emory University School of Medicine have found that deleting a certain gene in mice can improve their learning and memory abilities. The RGS14 gene, which is primarily active in one region of the hippocampus, appears to limit some forms of learning and memory when present.
Scientists have identified a new area of the brain that generates excitatory neurons in adults, which arise from non-neuronal support cells. This finding has significant implications for regenerative medicine and may lead to new treatments for brain injuries or disorders.
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A recent study published in the journal Brain has found a link between nerve cell production and memory in humans. The research suggests that increasing nerve cell regeneration in the hippocampus may alleviate or prevent memory loss, providing new insights into age-related cognitive decline.
A study published in Neuron reveals that GABA, a natural molecule in the brain, is responsible for regulating synaptic connections and facilitating the formation of new memories. The research demonstrates that variations in local GABA levels near individual synapses determine synaptic strength and heterogeneity.
Researchers at UT Southwestern Medical Center discovered a compound called P7C3 that preserves newly created brain cells and boosts learning and memory in animal studies. The study found that P7C3 protects newborn neurons from dying, restoring normal structure and function of the hippocampus in knockout mice.
A study by UT Southwestern Medical Center researchers found that APOE4 interferes with brain cell recycling of surface receptors, increasing Alzheimer's disease risk. The harmful molecule prevents the Reelin-binding receptor from being recycled back to the surface.
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Research from neuroscientist Samuel Weiss shows that paternal mice physically interact with their babies grow new brain cells and form lasting memories of their babies. The study demonstrates a positive feedback loop between social interactions and healthy brains.
Researchers discovered that neuronal stem cells exist in the human brain, even in adulthood, and can form new neurons. Physical activity and pathological stimuli like epileptic seizures reactivate dormant stem cells, promoting the formation of new neurons.
Scientists discovered that brain tissue produces a natural form of the clot-busting drug tPA, which acts as a neuroprotectant and may prevent strokes. The finding suggests a potential new approach to preventing ischemic stroke by prolonging the effects of naturally produced tPA.
The protein tPA provides protection for nerve cells in the hippocampus by preventing death caused by reduced blood flow during stroke. Analysis of tPA's protective process reveals implications for therapeutic strategies to prevent nerve cell death.
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Researchers found that fragile X protein (FMRP) regulates adult neurogenesis, a process crucial for learning and memory. FMRP dysregulation leads to defective neural maturation and reduced new neurons, contributing to learning disabilities associated with fragile X syndrome.
UT Southwestern researchers discovered that new brain nerve cells play a crucial role in stress resilience. Mice susceptible to stress exhibited enhanced neurogenesis, with surviving cells surviving longer than those produced by resilient mice.
Researchers at University of California - Berkeley found an insulin-like signal necessary to keep stem cells alive in the adult brain. Blocking apoptosis genes alone is not enough, as neural stem cells also require an insulin-type signal to persist. The study suggests that manipulating the insulin pathway may be essential for re-growin...
UCI researchers found that learning activates neuron receptors that promote brain growth and limit memory impairment associated with aging. The study suggests that staying mentally active as we age may keep neuronal BDNF signaling at a constant rate, limiting cognitive decline.
Researchers at Gladstone Institute of Neurological Disease have discovered that two main causes of AD, amyloid-beta peptides and apolipoprotein E4, impair the growth of new neurons born in adult brains. Drug treatments can normalize their development even in the presence of these factors.
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Researchers discovered that the peptide C3a regulates nerve cell maturation and migration in mice, which could lead to treating stroke, Parkinson's disease, and other neurological disorders. The study found that molecules similar to C3a can boost nerve cell formation and replace damaged cells.
Scientists found a newly discovered gene, KIAA1212, linking to schizophrenia and autism susceptibility genes. They successfully 'rescued' damaged brain cells using rapamycin, a drug acting on mTOR protein.
Researchers at UT Southwestern Medical Center found that applying a second brain protein, Reelin, can prevent excess beta-amyloid from silencing nerves and potentially fighting Alzheimer's disease. The study suggests a promising new tactic against the devastating illness.
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Two studies found that the DISC1 gene regulates neuronal development by interacting with Girdin, an actin-binding protein. Disrupted interactions lead to abnormal neurogenesis and a disorganized hippocampus. Pharmacological inhibition of mTOR rescues defects in neuronal development.
Researchers used pictures, spoken and written names to show that single neurons in the human hippocampus and surrounding areas respond selectively to representations of the same individual using different sensory prompts. This process enables abstraction and recognition of highly variable images.
Researchers have devised a chemical technique to discover brain function and provide clues for treating brain diseases. The technique allows neuroscientists to noninvasively activate entire populations of neurons in an animal brain, promoting understanding of brain function and disease treatment.
Researchers discovered that newborn neurons in the hippocampus help separate individual events and form temporal relationships, improving spatial memory. This breakthrough sheds light on the purpose of neurogenesis and its role in adult brain function.
A study on rats reveals that neural replay of past experiences occurs both during and after wakefulness, forming long-term memories more accurately. The hippocampus replays events in peppered bursts, often involving different settings, suggesting elements of past experience are constantly reactivated.
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Cold Spring Harbor Laboratory researchers discovered that oligophrenin-1 (OPHN1) is crucial for neural signaling by controlling the recycling of synaptic vesicles. Defective OPHN1 signaling leads to misshapen dendritic spines and loss of synaptic strength, contributing to X-linked mental retardation.
Researchers found that 50% of hippocampal cells differentiate between correct and incorrect responses, influencing new learning by changing cell sensitivity. The study establishes a physiological link between associative learning and processing trial outcomes.
New study finds stress-related changes in brain structure may lead to depression-like behavior and PTSD. Researchers propose that restoring hippocampal synapses could provide immediate relief from depressive symptoms.
Researchers found synchronous neuron pairs firing in harmony during slow-wave sleep, but not during REM sleep, which may explain why dreams are difficult to remember. This discovery provides a framework for further research into the relationship between memory and sleep.
A computational model suggests that newborn brain cells add a unique time-related code to memories formed around the same time. This allows for recall of events from a certain period and connects independent events that occurred during the same hyperactive period, explaining why memories can be triggered by specific details.
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Researchers at Northwestern University have discovered a new cellular mechanism that requires both types of neuronal metabotropic receptors to produce biochemical changes, increasing neuron firing and strengthening signals to other brain regions.
A study by Chen et al. reveals that chopped-up ECM triggers excitotoxicity through the kainate receptor's KA1 subunit, leading to brain damage. Drugs blocking KA1 might provide an alternative way to save brain cells after stroke or head trauma without causing cognitive impairment.
Researchers found PSD-95 stimulates the growth of large dendritic spines that are connected to multiple axons. Reducing PSD-95 levels impairs synapse development.
Researchers led by Prof. Itzhak Fried discovered that the same neurons excited during an experience are also activated when remembering it, providing a clearer picture of how memory recall works. This finding has important implications for understanding dementias like Alzheimer's.
A new study confirms that exercise can reverse the age-related decline in neural stem cells in the hippocampus of mouse brains. Exercise restores a brain chemical promoting new stem cell production and maturation.
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A study found that inactivating a specific gene in adult neural stem cells causes nerve cells to form connections in the wrong part of the brain. The research suggests that cdk5, a protein necessary for correct neuron development, is essential for accurate maturation of newborn granule cells.
Researchers at the Salk Institute found that a protein called cdk5 is necessary for correct neural migration and dendritic pathfinding in adult brains. Disabling cdk5 made newborn neurons form connections in the wrong part of the brain, with inappropriate synaptic connections persisting for months after treatment.
Scientists have identified a missing-link molecule that explains the process of plasticity and could lead to targeted therapies for learning and memory. The discovery of myosin Vb, a molecular motor, reveals its role in delivering new receptors to synapses, strengthening connections between nerve cells.
Researchers at the Salk Institute discovered that the signal transmission between neurons in the brain stem, which controls balance and breathing, is linear, unlike most other signals. The study sheds light on the mechanisms controlling these vital functions and may lead to new biotherapeutic agents.
Scientists at UCLA and the Weizmann Institute of Science recorded individual brain cells as they recalled memories from epilepsy patients' brains. The study confirms that spontaneous memories arise with activity of the same neurons that were recorded as they fired when the memory was first being made.
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The adult brain's capacity for neurogenesis is closely tied to stress and depression, with research showing that chronic stress can inhibit new cell growth in the hippocampus. However, antidepressant treatment has been shown to stimulate neurogenesis, suggesting a potential therapeutic target for treating major depressive disorders.
A functional link between new neuron production and antidepressant effectiveness has been discovered in an animal model. TrkB-mediated neural proliferation plays a crucial role in this mechanism, supporting the notion that impaired neurogenic niches contribute to refractory responses to antidepressive treatments.
A new UNC study reveals that stopping moderate drinking may lead to health problems, including depression and reduced brain capacity. Treatment with antidepressant drugs can prevent the development of depression and restore brain function.
A study found that Ritalin works in the prefrontal cortex to enhance cognition and focus, while having limited effects elsewhere. The medication tunes neuron sensitivity to signals, leading to improved cognitive function and attention.