Research Keyword: neurodegeneration

Dietary live microbe intake and its association with Parkinson’s disease in American adults: an NHANES analysis (1999–2018)

This study found that eating more foods rich in live microbes—like fermented products (yogurt, kimchi) and fresh fruits and vegetables—is associated with lower rates of Parkinson’s disease in American adults. The protective effect was strongest in people without obesity. The live microbes appear to work by maintaining a healthy gut environment, reducing inflammation, and protecting nerve cells from damage. This suggests that regular consumption of microbe-rich foods from nature might be a simple, inexpensive way to help prevent or slow Parkinson’s disease.

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Investigating the Neuroprotective, Hepatoprotective, and Antimicrobial Effects of Mushroom Extracts

This study examined four types of edible mushrooms to see if they could protect against aging and fight harmful bacteria. Researchers gave mice an aging-inducing substance and then treated them with mushroom extracts. The mushrooms, particularly Lion’s Mane (Hericium erinaceus), helped prevent brain and liver damage, reduced inflammation, and showed antibacterial effects against multiple bacterial strains. These findings suggest mushrooms could be useful natural supplements to promote health and combat age-related decline.

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Neuroprotective Effect of Mixed Mushroom Mycelia Extract on Neurotoxicity and Neuroinflammation via Regulation of ROS-Induced Oxidative Stress in PC12 and BV2 Cells

A mixture of three medicinal mushrooms (Phellinus linteus, Ganoderma lucidum, and Inonotus obliquus) was tested for its ability to protect nerve cells from damage. The extract successfully reduced cell death in laboratory models of neurodegeneration by reducing harmful molecules called reactive oxygen species and reducing inflammation. These results suggest the mushroom extract could potentially help prevent or slow neurological diseases like Alzheimer’s.

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Screening of active components of Ganoderma lucidum and decipher its molecular mechanism to improve learning and memory disorders

Researchers used computer analysis and laboratory experiments to understand how a medicinal mushroom called Ganoderma lucidum (reishi) helps improve memory and learning problems. They identified ten key active ingredients in the mushroom that work together to reduce inflammation in the brain and protect nerve cells. The most important ingredient appears to be a compound called β-sitosterol, which helps prevent memory loss similar to effects seen in Alzheimer’s disease.

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Safety, feasibility, and tolerability of psilocybin in older adults with amnestic MCI: Preliminary data from a SV2a PET imaging study

Researchers investigated whether psilocybin, a compound from certain mushrooms, could be safely used to treat memory problems in older adults with mild cognitive impairment. In this early-stage study, participants received either psilocybin or a placebo while researchers used brain imaging to measure changes in synaptic connections. The preliminary results suggest psilocybin was well-tolerated with manageable side effects like dizziness, and participants were able to complete the study without serious problems.

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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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Impaired spatial memory in adult vitamin D deficient BALB/c mice is associated with reductions in spine density, nitric oxide, and neural nitric oxide synthase in the hippocampus

This study found that adults with vitamin D deficiency have impaired spatial memory and reduced brain structures called dendritic spines in the hippocampus, the brain region responsible for learning and memory. The researchers identified that low vitamin D decreases nitric oxide production in the brain, which is important for forming and maintaining the synaptic connections needed for memory formation. Importantly, when vitamin D was supplemented back to deficient mice, the brain’s ability to produce nitric oxide was restored, suggesting vitamin D supplementation could potentially improve cognitive function in vitamin D-deficient individuals.

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Hericioic Acids A–G and Hericiofuranoic Acid; Neurotrophic Agents from Cultures of the European Mushroom Hericium flagellum

Researchers isolated eight new bioactive compounds from a rare European mushroom species called Hericium flagellum. These compounds showed promising ability to stimulate nerve cell growth and could potentially help treat neurodegenerative diseases like Alzheimer’s and Parkinson’s. The study demonstrates that mushroom-derived natural products may offer new therapeutic approaches for conditions affecting millions of elderly people worldwide.

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Strain-specific effects of Desulfovibrio on neurodegeneration and oxidative stress in a Caenorhabditis elegans PD model

This research shows that different strains of bacteria called Desulfovibrio have very different effects on brain health. When scientists exposed worms to six different strains, they found that environmental strains actually protected against Parkinson’s-like symptoms, while strains from human patients and animals caused more damage. The worms strongly preferred to eat the environmental strains, suggesting they could sense which bacteria were harmful. This highlights how the type of bacteria in our gut matters just as much as the total amount.

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

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.

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