neuroinflammation – Page 3

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

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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.

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

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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.

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

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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.

Microbial links to Alzheimer’s disease

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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.

Butyrate ameliorates quinolinic acid–induced cognitive decline in obesity models

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This research shows that overweight and obese individuals have higher levels of a toxic compound called quinolinic acid in their bodies, which is linked to memory problems and brain shrinkage. The good news is that butyrate, a substance naturally produced by gut bacteria when we eat fiber, can protect against these harmful effects. Butyrate works by activating genes that produce brain-derived neurotrophic factor (BDNF), a protein essential for brain health and memory formation. The study suggests that increasing butyrate through diet or supplements could help prevent cognitive decline associated with obesity.

N6-methyladenosine-modified circRIMS2 mediates synaptic and memory impairments by activating GluN2B ubiquitination in Alzheimer’s disease

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This research reveals how an abnormal RNA molecule called circRIMS2 contributes to Alzheimer’s disease by damaging brain synapses and impairing memory. Scientists found that circRIMS2 levels are elevated through a chemical modification called m6A methylation, and this causes a cascade of events leading to the destruction of important proteins needed for brain communication. The study shows that blocking this damaging pathway using a specially designed peptide can restore memory and synaptic function in Alzheimer’s disease models, offering hope for new therapeutic approaches.

Long term worsening of amyloid pathology, cerebral function, and cognition after a single inoculation of beta-amyloid seeds with Osaka mutation

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Researchers found that a single exposure to mutated amyloid-beta proteins (Aβ Osaka) in the brains of genetically modified mice caused lasting damage over four months. The mutated proteins triggered more severe memory loss, brain connectivity problems, and synapse damage compared to normal amyloid-beta. This suggests that even one encounter with mutated amyloid proteins can set off a chain reaction of disease progression that persists long after initial exposure.

Microbial links to Alzheimer’s disease

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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.

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

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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.

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

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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.

Research Keyword: neuroinflammation