Over the past year, three people with paralysis have received Neuralink implants. This blog post explores how each person is using Telepathy in everyday life.
Category: neuroscience
Dr. Wang joined the Max Planck Florida Institute for Neuroscience (MPFI) in February 2018 leading the Neuronal Mechanisms of Episodic Memory research group
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Before joining MPFI, Wang was a research scientist at the Janelia Research Campus of Howard Hughes Medical Institute, working with Dr. Jeffery Magee and previously with Dr. Eva Pastalkova. At Janelia, she studied the hippocampal neuronal activities that represent memory traces. In particular, she employed memory tasks that can reversibly toggle the influence of sensory inputs on and off and isolated neuronal activities associated with internally stored memory.
Wang was trained as an electrical engineer. She completed her graduate study under the mentorship of Drs. Shih-Chii Liu, Tobi Delbruck and Rodney Douglas at the Swiss Federal Institute of Technology Zurich (ETHZ). During her Ph.D. training, she designed brain-inspired computational systems on silicon chips. These fully reconfigurable systems incorporated electronic circuits of a network of neurons with dendrites and synapses. Using these systems as simulation tools, she also investigated the computational principles native to a neuron with active dendrites.
Gardenias are known for their rich, earthy fragrance, waxy petals and brilliant white color that contrasts with the deep emerald green of their leaves. The plant has long been prized by herbalists, seekers of food and fabric dyes, and even pharmaceutical companies.
Now, a collaborative team of scientists at several research centers in the United States has found that a compound known as genipin, derived from the gardenia plant called Cape jasmine, can prompt nerve regeneration. Neurons damaged and stunted by disease find new life in the lab when exposed to the plant-derived compound.
The chemical comes from the fruit of this extraordinarily versatile plant. Gardenia shrubs, in general, are native to tropical and subtropical regions of Asia. But the plants are propagated globally by horticulturists and amateur gardeners who are most familiar with the flower’s beauty and the intoxicating scent of their perfume.
Years before tau tangles show up in brain scans of patients with Alzheimer’s disease, a biomarker test developed at the University of Pittsburgh School of Medicine can detect small amounts of the clumping-prone tau protein and its misfolded pathological forms that litter the brain, cerebrospinal fluid and potentially blood, new research published today in Nature Medicine suggests.
The cerebrospinal fluid biomarker test correlates with the severity of cognitive decline, independent of other factors, including brain amyloid deposition, thereby opening doors for early-stage disease diagnosis and intervention.
Since amyloid-beta pathology often precedes tau abnormalities in Alzheimer’s disease, most biomarker efforts have focused on early detection of amyloid-beta changes. However, the clumping of tau protein into well-ordered structures referred to by pathologists as “neurofibrillary tangles” is a more defining event for Alzheimer’s disease as it is more strongly associated with the cognitive changes seen in affected people.
Frontiers: Cellular aging is a multifactorial and intricately regulated physiological process with profound implications
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The interaction between cellular senescence and cancer is complex and multifaceted, senescence can both promote and inhibit tumor progression through various mechanisms. M6A methylation modification regulates the aging process of cells and tissues by modulating senescence-related genes. In this review, we comprehensively discuss the characteristics of cellular senescence, the signaling pathways regulating senescence, the biomarkers of senescence, and the mechanisms of anti-senescence drugs. Notably, this review also delves into the complex interactions between senescence and cancer, emphasizing the dual role of the senescent microenvironment in tumor initiation, progression, and treatment. Finally, we thoroughly explore the function and mechanism of m6A methylation modification in cellular senescence, revealing its critical role in regulating gene expression and maintaining cellular homeostasis. In conclusion, this review provides a comprehensive perspective on the molecular mechanisms and biological significance of cellular senescence and offers new insights for the development of anti-senescence strategies.
Cellular senescence is a complex and multifaceted biological process characterized by a stable arrest of the cell cycle in response to various stressors, such as DNA damage, oxidative stress, and oncogene activation (1). Although senescent cells no longer proliferate, they remain metabolically active and exhibit distinct phenotypic changes, including the secretion of pro-inflammatory factors, collectively termed the senescence-associated secretory phenotype (SASP) (2, 3). Senescence plays dual roles in physiological and pathological contexts: it is essential for processes like tissue remodeling, wound healing, and tumor suppression, yet its accumulation contributes to aging, chronic inflammation, and the progression of age-related diseases, including cancer and neurodegenerative disorders (4). Understanding the mechanisms underlying cellular senescence is crucial for developing therapeutic strategies to harness its beneficial aspects while mitigating its detrimental effects.
Synaptic vesicles (SVs) store and transport neurotransmitters to the presynaptic active zone for release by exocytosis. After release, SV proteins and excess membrane are recycled via endocytosis, and new SVs can be formed in a clathrin-dependent manner. This process maintains complex molecular composition of SVs through multiple recycling rounds. Previous studies explored the molecular composition of SVs through proteomic analysis and fluorescent microscopy, proposing a model for an average SV. However, the structural heterogeneity and molecular architecture of individual SVs are not well described. Here, we used cryoelectron tomography to visualize molecular details of SVs isolated from mouse brains and inside cultured neurons. We describe several classes of small proteins on the SV surface and long proteinaceous densities inside SVs.
Summary: Researchers have discovered that positive emotions enhance perceptual memories during sleep, particularly in the non-REM stage. Using mice, they found that memories linked to rewarding experiences lasted longer than neutral ones. The amygdala plays a key role in strengthening these memories by activating a tri-regional circuit with the motor and sensory cortices.
Brain recordings confirmed that this circuit reactivates during non-REM sleep, solidifying perceptual memories. Blocking amygdala signals during non-REM sleep disrupted memory retention, while blocking them during REM sleep had no effect. These findings suggest new ways to treat conditions like addiction and PTSD by targeting non-REM sleep processes.
A study confirms the positive effects of exercise on insulinInsulin is a hormone produced by the pancreas, crucial for regulating blood glucose levels. It helps cells in the body absorb glucose from the bloodstream and convert it into energy or store it for future use. Insulin production and action are essential for maintaining stable blood sugar levels. In people with diabetes, the body either does not produce enough insulin (Type 1 diabetes) or cannot effectively use the insulin it does produce (Type 2 diabetes), leading to elevated levels of glucose in the blood. This can cause various health complications over time, including heart disease, kidney damage, and nerve dysfunction. Insulin therapy, where insulin is administered through injections or an insulin pump, is a common treatment for managing diabetes, particularly Type 1. The discovery of insulin in 1921 by Frederick Banting and Charles Best was a landmark in medical science, transforming diabetes from a fatal disease to a manageable condition. tabindex=0 insulin signaling proteins in the brain.
New research reveals that disrupted sleep may be the hidden link between heavy cannabis use and memory deficits, unmasking an unexpected culprit behind cognitive impairments.
Advances in brain-computer interfaces enable paralysed users to feel objects in a realistic way via a robotic limb.