stroke tagged posts

New finding on Elusive Brain Receptor sheds light on what may Kill Neurons after Stroke

N3A receptor site

The N3A receptor, as modeled here by the UB researchers, may be silent under normal conditions, but can be reactivated through the unique site (in red) under acidic conditions, such as after a stroke or seizure.

Strokes, seizures, traumatic brain injury and schizophrenia: these conditions can cause persistent, widespread acidity around neurons in the brain. But exactly how that acidity affects brain function isn’t well understood. University at Buffalo researchers have begun to unravel some of the puzzle. They found that an elusive brain receptor may play an important role in the death of neurons from neurological diseases.

The UB researchers study a family of brain receptors that are critical to learning and memory, called NMDA (N-methyl-D-aspartate) receptors...

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Certain GI Bacteria leverage the Immune system to Decrease the Severity of Stroke

Immune cells (green) assemble in the outer coverings of a mouse's brain, called the meninges, protecting it from a stroke's full force. Gut bacteria modified the immune' cells behavior to elicit that protective response. Credit: Corinne Benakis

Immune cells (green) assemble in the outer coverings of a mouse’s brain, called the meninges, protecting it from a stroke’s full force. Gut bacteria modified the immune’ cells behavior to elicit that protective response. Credit: Corinne Benakis

New research from Weill Cornell Medicine can help mitigate stroke – the second leading cause of death worldwide. In the study mice received a combination of antibiotics. 2 weeks later, ischemic stroke was induced in them. Mice treated with antibiotics experienced a stroke that was about 60% smaller than rodents that did not receive the medication. The microbial environment in the gut directed the immune cells there to protect the brain from the stroke’s full force.

Modifying the microbiotic makeup of the gut can become an innovative method to preven...

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Gut Microbes influence Platelet function, risk of Thrombosis

Highlights •Elevated TMAO levels predict incident risk for thrombotic events in human subjects •TMAO enhances sub-maximal stimulus-dependent platelet activation •Dietary choline, gut microbes, and TMAO are linked to thrombotic potential in vivo •Microbial transplantation shows that thrombosis potential is a transmissible trait

Highlights •Elevated TMAO levels predict incident risk for thrombotic events in human subjects •TMAO enhances sub-maximal stimulus-dependent platelet activation •Dietary choline, gut microbes, and TMAO are linked to thrombotic potential in vivo •Microbial transplantation shows that thrombosis potential is a transmissible trait

TMAO – gut byproduct of animal-rich diets – encourages over-reactive platelet function, increasing thrombosis risk. In a combination of both clinical studies of over 4,000 patients and animal model studies, Cleveland Clinic researchers have demonstrated – for the first time – that gut microbes alter platelet function and risk of blood clot-related illnesses like heart attack and stroke.

When the nutrient choline –which is abundant in animal products like meat...

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How a Waste Product of Exercise Protects Neurons from Trauma Damage

(1) Excessive glutamate activity triggers a strong influx of calcium (Ca2+) into the neuron through NMDA receptors, which leads to cell death. (2) Lactate is transported into the neuron and (3) converted to pyruvate by the enzyme lactate dehydrogenase (LDH). (4) Pyruvate is then transported into mitochondria by the mitochondrial pyruvate carrier (MPC) where it generates ATP. (5) ATP is then released through pannexins and activates the receptor P2Y, which (6) activates the PI3K pathway. (7) This triggers the opening of potassium channels (K+), which causes the neuron to hyperpolarize, decreasing the neuron's excitability, and thus protecting it from excitotoxic damage.

(1) Excessive glutamate activity triggers a strong influx of calcium (Ca2+) into the neuron through NMDA receptors, which leads to cell death. (2) Lactate is transported into the neuron and (3) converted to pyruvate by the enzyme lactate dehydrogenase (LDH). (4) Pyruvate is then transported into mitochondria by the mitochondrial pyruvate carrier (MPC) where it generates ATP. (5) ATP is then released through pannexins and activates the receptor P2Y, which (6) activates the PI3K pathway. (7) This triggers the opening of potassium channels (K+), which causes the neuron to hyperpolarize, decreasing the neuron’s excitability, and thus protecting it from excitotoxic damage.

Researchers led by EPFL have found how lactate, a waste product of glucose metabolism can protect neurons from damage follo...

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