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Category: neuroscience – Page 8

Sylvain Lesné, a neuroscientist accused of image manipulation in a seminal Alzheimer’s disease paper in, resigned last week from his tenured professorship at the University of Minnesota Twin Cities (UMN). The move follows a 2.5-year investigation in which the university found problems with several other papers on which Lesné is an author. The study has already been pulled, but the school has asked that four more of Lesné’s papers be retracted.

The resignation, effective 1 March, was first reported by the. Lesné did not respond to a request for comment. UMN spokesperson Jake Ricker said, “The university has identified data integrity concerns impacting several publications and has been in touch with those journals to recommend retraction of the publications, where appropriate.”

As a postdoc, Lesné worked in the lab of neuroscientist Karen Ashe. In 2006, they published a study in that seemed to show a cause-effect relationship between a protein—amyloid-beta *56—and memory loss in rats. Those symptoms seemed to resemble the memory problems that afflict Alzheimer’s patients.

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Imagine a world where your thoughts aren’t confined to the boundaries of your skull, where your consciousness is intimately connected to the universe around you, and where the neurons in your brain communicate instantly across vast distances.

This isn’t science fiction — it’s the intriguing possibility suggested by applying the principle of quantum entanglement to the realm of consciousness.

Quantum entanglement, often described as the “spooky action at a distance,” is a phenomenon that baffled even Einstein. In essence, it describes a scenario where two particles become so deeply linked that they share the same fate, regardless of the distance separating them. Measuring the state of one instantly reveals the state of its partner, even if they are light-years apart.

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Scientists explored Human Accelerated Regions (HARs), genetic regulators that tweak existing genes rather than introducing new ones. Using cutting-edge techniques, they mapped nearly all HAR interactions, revealing their role in brain development and neurological disorders like autism and schizophrenia.

Decoding the Genetic Evolution of the Human Brain

A new Yale study offers a deeper understanding of the genetic changes that shaped human brain evolution and how this process differed from that of chimpanzees.

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Our guts are home to trillions of bacteria, and research over the last few decades has established how essential they are to our physiology—in health and disease. A new study from EMBL Heidelberg researchers shows that gut bacteria can bring about profound molecular changes in one of our most critical organs—the brain.

The new study, published in the journal Nature Structural & Molecular Biology, is the first to show that bacteria living in the gut can influence how proteins in the brain are modified by carbohydrates—a process called glycosylation. The study was made possible by a new method the scientists developed—DQGlyco—which allows them to study glycosylation at a much higher scale and resolution than previous studies.

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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.

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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.

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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 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 “” is a more defining event for Alzheimer’s disease as it is more strongly associated with the cognitive changes seen in affected people.

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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.

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