synaptic plasticity – Page 4

β-secretase inhibition prevents structural spine plasticity deficits in AppNL-G-F mice

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Researchers tested whether a drug that blocks BACE1 (an enzyme involved in Alzheimer’s disease) could protect nerve cell connections in a mouse model of Alzheimer’s disease. They found that at high doses, the drug significantly improved the formation of new dendritic spines (connection points between neurons) and restored synaptic activity to near-normal levels. These findings suggest that using BACE1 inhibitors early in Alzheimer’s disease development, before widespread neuronal damage occurs, might help prevent cognitive decline.

Cerebral Hypoxia-Induced Molecular Alterations and Their Impact on the Physiology of Neurons and Dendritic Spines: A Comprehensive Review

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This review explains how low oxygen levels in the brain damage nerve cells and their connection points (dendritic spines) through a cascade of molecular changes. The brain normally has protective mechanisms, but severe or prolonged hypoxia overwhelms these defenses, leading to memory loss and cognitive problems. Several molecular pathways and supporting cells called astrocytes and microglia can help protect neurons. Understanding these protective mechanisms may lead to new treatments for brain conditions caused by low oxygen, such as stroke.

Primary cilia in the mature brain: emerging roles in Alzheimer’s disease pathogenesis

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Primary cilia are small hair-like structures on brain cells that act like sensory antennas, helping regulate memory and thinking ability. In Alzheimer’s disease, these structures become abnormally shaped and function poorly, contributing to memory loss and cognitive decline. The shape and function of primary cilia change as the brain ages and when amyloid plaques develop, suggesting they could be targeted with new treatments to slow Alzheimer’s progression.

New Positive TRPC6 Modulator Penetrates Blood–Brain Barrier, Eliminates Synaptic Deficiency and Restores Memory Deficit in 5xFAD Mice

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Researchers developed a new drug candidate called C20 that activates TRPC6 proteins in the brain. In studies with Alzheimer’s disease mouse models, C20 protected nerve connections from damage, restored memory function, and successfully crossed the blood-brain barrier. The compound shows promise as a potential treatment for Alzheimer’s disease by strengthening the connections between brain cells that are damaged in the disease.

Reprogramming astrocytic NDRG2/NF-κB/C3 signaling restores the diabetes-associated cognitive dysfunction

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This study found that regular exercise helps protect the brain of diabetic people from cognitive decline by boosting a protein called NDRG2 in astrocytes (brain support cells). The research shows that NDRG2 works by blocking harmful immune responses that damage synapses (connections between brain cells). In diabetic mice, exercise improved memory and learning ability while increasing NDRG2 levels, while blocking this protein reversed these benefits.

Three Different Types of β-Glucans Enhance Cognition: The Role of the Gut-Brain Axis

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Researchers tested three types of β-glucans—fiber compounds found in mushrooms, oats, and other foods—to see if they could improve memory in mice. All three types enhanced recognition memory and reduced brain inflammation, while only oat β-glucan significantly changed gut bacteria composition. The findings suggest that different β-glucans may help prevent cognitive decline through different mechanisms involving the gut-brain connection.

Rac1/PAK1 signaling contributes to bone cancer pain by regulation dendritic spine remodeling in rats

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Researchers studied how bone cancer pain develops in rats and found that a specific cellular signaling pathway called Rac1/PAK1 plays a key role. When tumors grow in bone, this pathway becomes overactive and causes changes in nerve cell structures called dendritic spines, which leads to increased pain sensitivity. By blocking this pathway with a drug called NSC23766, scientists were able to reduce pain and reverse the harmful changes to nerve cells, suggesting a new potential treatment approach for cancer patients suffering from bone pain.

Conditional deletion of ROCK2 induces anxiety-like behaviors and alters dendritic spine density and morphology on CA1 pyramidal neurons

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Researchers created mice with reduced ROCK2 protein in brain cells to understand how this protein affects behavior and brain structure. These mice showed anxiety-like behavior, avoiding open spaces and preferring darkness. The study found that ROCK2 affects the structure of dendritic spines, which are tiny branches on nerve cells that allow communication between neurons, particularly in the hippocampus region involved in learning and memory.

Research Keyword: synaptic plasticity