Research Topic: neuroinflammation

Sporoderm-removed ganoderma lucidum spore powder (S-GLSP) alleviates neuroinflammation injury by regulating microglial polarization through inhibition of NLRP3 inflammasome activation

Researchers found that sporoderm-removed Ganoderma lucidum spore powder (S-GLSP) protects against Alzheimer’s disease by reducing brain inflammation. The supplement works by shifting immune cells in the brain called microglia from a harmful pro-inflammatory state to a protective anti-inflammatory state. This is accomplished by blocking the NLRP3 inflammasome, a key trigger of brain inflammation. In animal and cell studies, S-GLSP improved memory, reduced neuronal damage, and decreased harmful tau protein accumulation.

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Microglia and astrocytes mediate synapse engulfment in a MER tyrosine kinase-dependent manner after traumatic brain injury

After a traumatic brain injury, brain cells called microglia and astrocytes overzealously consume synapses (connections between neurons), which prevents the brain from healing properly. This study shows that these brain cells use a specific protein called MERTK to do this unwanted cleanup. When researchers blocked MERTK in these cells, the mice recovered better motor and cognitive function, had smaller brain injuries, and maintained more healthy synapses.

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High-Fat Diet Consumption Induces Neurobehavioral Abnormalities and Neuronal Morphological Alterations Accompanied by Excessive Microglial Activation in the Medial Prefrontal Cortex in Adolescent Mice

This study shows that eating a high-fat diet during the teenage years can harm brain development and mood in mice. The research found that high-fat diets led to anxiety and depression-like symptoms, along with shrinking brain structures and overactive immune cells in the brain. These findings suggest that teenagers should maintain healthy eating habits, as poor diet during adolescence may have long-lasting effects on mental health.

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Assessment of Lab4P Probiotic Effects on Cognition in 3xTg-AD Alzheimer’s Disease Model Mice and the SH-SY5Y Neuronal Cell Line

Researchers tested a probiotic supplement called Lab4P on mice genetically engineered to develop Alzheimer’s-like symptoms and on human brain cells exposed to damaging proteins. The supplement successfully improved memory and cognitive function in the mice while protecting brain cells from damage, with stronger benefits when the mice were also on a high-fat diet. These findings suggest that probiotics might help prevent or slow cognitive decline related to Alzheimer’s disease.

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Microbial links to Alzheimer’s disease

Researchers are investigating whether common infections from bacteria, viruses, and fungi might trigger or worsen Alzheimer’s disease. Studies show that pathogens like the bacteria that causes gum disease and certain herpes viruses can reach the brain and trigger inflammation and amyloid-beta accumulation, key features of Alzheimer’s. While the evidence is promising, scientists haven’t yet proven whether these infections cause Alzheimer’s or simply make existing disease worse.

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Microbial links to Alzheimer’s disease

This review examines whether germs like bacteria, fungi, and viruses might play a role in causing Alzheimer’s disease. Scientists have found that certain bacteria from the mouth and gut, fungal infections, and cold sores (herpes viruses) appear more frequently in Alzheimer’s patients and may trigger the brain changes that damage memory and thinking. While the evidence is promising, researchers still need to determine whether these infections actually cause Alzheimer’s or simply make it worse once it develops.

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β-chitosan attenuates hepatic macrophage-driven inflammation and reverses aging-related cognitive impairment

Researchers found that β-chitosan, a compound extracted from squid parietal bone, can reverse age-related memory and learning problems in mice, zebrafish, and worms. The compound works by reducing excessive inflammation in the liver and lowering inflammatory chemicals in the blood, which in turn reduces brain inflammation. This discovery suggests a direct connection between liver health and brain aging, and β-chitosan may offer a new therapeutic approach for age-related cognitive decline.

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The Biological Activity of Ganoderma lucidum on Neurodegenerative Diseases: The Interplay between Different Active Compounds and the Pathological Hallmarks

Reishi mushroom, used in traditional Asian medicine for centuries, contains over 400 bioactive compounds that show promise in protecting the brain from degenerative diseases like Alzheimer’s and Parkinson’s. The mushroom’s components work through multiple pathways to reduce inflammation, fight oxidative stress, and protect neurons from damage. While laboratory and animal studies show encouraging results, human clinical trials are needed to confirm its effectiveness as a treatment.

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

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.

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Mechanisms of Talaromyces marneffei induced CNS injury: Synergistic roles of tauopathy, pyroptosis, and microglial inflammation

A dangerous fungus called Talaromyces marneffei can invade the brain and cause serious damage in people with weakened immune systems. The study shows the fungus harms brain cells through two pathways: direct damage to neurons and indirect damage through activation of brain immune cells that release harmful inflammatory chemicals. Understanding these mechanisms could help develop better treatments for this life-threatening infection.

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