Research Keyword: cognitive decline

Fungal Bioactive Compounds as Emerging Therapeutic Options for Age-Related Neurodegenerative Disorders

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Mushrooms contain special compounds that may help protect our brains as we age. These fungal compounds fight inflammation, reduce harmful free radicals, and help clear out damaged cellular parts—all things that slow down brain aging and diseases like Alzheimer’s and Parkinson’s. While the research looks very promising in lab and animal studies, scientists still need to figure out how to make these compounds work better in the human body and prove they’re safe and effective in patients.

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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

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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.

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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.

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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.

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GDF11 slows excitatory neuronal senescence and brain ageing by repressing p21

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As we age, brain cells called excitatory neurons undergo senescence, similar to cellular ageing. This study found that a protein called GDF11 protects these neurons from ageing. When GDF11 was removed from excitatory neurons in mice, the neurons aged faster, leading to memory problems and shorter lifespans. The research reveals that GDF11 works by blocking p21, a molecule that promotes cellular ageing.

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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.

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