amyloid-beta – mycolab.ai

Screening of a Fraction with Higher Amyloid β Aggregation Inhibitory Activity from a Library Containing 210 Mushroom Extracts Using a Microliter-Scale High-Throughput Screening System with Quantum Dot Imaging

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Researchers screened 210 mushroom species from Japan to find those that could prevent harmful protein clumping in the brain associated with Alzheimer’s disease. They identified a purified fraction from the mushroom Elfvingia applanata that was more effective than a known anti-Alzheimer’s compound at stopping these protein clumps from forming. The extract also protected nerve cells from damage in laboratory tests. This finding suggests mushrooms could potentially be developed into a functional food to help prevent Alzheimer’s disease.

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

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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.

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.

Neuroprotective properties of anti-apoptotic BCL-2 proteins in 5xFAD mouse model of Alzheimer’s disease

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Scientists studied how Bcl-2 proteins might protect the brain from Alzheimer’s disease by controlling calcium levels in nerve cells. They injected modified Bcl-2 proteins into the brains of mice engineered to develop Alzheimer’s symptoms and found that these proteins helped preserve the connections between nerve cells and reduced harmful amyloid plaque buildup. A special version of Bcl-2 that worked primarily on one type of calcium channel was surprisingly most effective at reducing amyloid plaques, suggesting this specific mechanism could be important for treating Alzheimer’s disease.

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.

Identification of potential neuroprotective compound from Ganoderma lucidum extract targeting microtubule affinity regulation kinase 4 involved in Alzheimer’s disease through molecular dynamics simulation and MMGBSA

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Researchers used computer simulations to test five compounds from Reishi mushrooms against Alzheimer’s disease. They found that two compounds, ganoderic acid A and ganoderenic acid B, showed strong potential for blocking a harmful protein involved in the disease. These findings suggest Reishi mushrooms could be a source for new Alzheimer’s treatments, though further laboratory testing is needed.

Research Keyword: amyloid-beta

Screening of a Fraction with Higher Amyloid β Aggregation Inhibitory Activity from a Library Containing 210 Mushroom Extracts Using a Microliter-Scale High-Throughput Screening System with Quantum Dot Imaging

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

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

Microbial links to Alzheimer’s disease

Neuroprotective properties of anti-apoptotic BCL-2 proteins in 5xFAD mouse model of Alzheimer’s disease

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

Identification of potential neuroprotective compound from Ganoderma lucidum extract targeting microtubule affinity regulation kinase 4 involved in Alzheimer’s disease through molecular dynamics simulation and MMGBSA