This new drug can prevent Alzheimer’s

A team of scientists has found a new drug that may prevent neuronal death through glucose metabolism modification in stressed neurons. The trials conducted on mice are rather promising for future use in humans. The new drug can be advantageous in neurological conditions ranging from Amyotrophic lateral sclerosis, Alzheimer's, and Huntington's diseases to traumatic brain injury and ischemic stroke.

According to WHO, stroke is the second most common cause of mortality, and more than a third of people who have survived a stroke will have a severe disability. As the population ages, many more millions are poised to develop Alzheimer's or Parkinson's diseases in the near future.

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Glycolysis is generally considered as the metabolic pathway essential for cell survival since it meets cell energy needs in case of intensive energy consumption. However, it is already known that in the brain tissue, the situation is quite different - different cell types show distinct glucose metabolism patterns.

In neurons, only a small portion of glucose is consumed via the glycolysis pathway. At the same time, astrocytes provide nutrients to neurons and utilize glycolysis to metabolise glucose. These differences are mostly due to the special protein called PFKFB3, which is normally absent in neurons and is active in astrocytes.

In the case of certain neurological diseases, stroke being one of them, the amount of active PFKFB3 increases in neurons, which is highly stressful for these cells and leads to cell death. Researchers in the in vivo experiments confirmed that a small molecule, the inhibitor of PFKFB3, may prevent cell death in the case of ischemia injury.

Inhibition of PFKFB3 improves motor coordination of mice after stroke and reduced brain infarct volume. Moreover, PFKFB3 inhibitor protects neurons from the amyloid-beta peptide, the main component of the amyloid plaques found in the brains of Alzheimer's disease patients.

Professor said, "Excitotoxicity is a hallmark of various neurological diseases, stroke being one of them. Our group has previously established a link between this pathological condition and high activity of PFKFB3 enzyme in neurons, which leads to severe oxidative stress and neuronal death"

"These promising results bring hope to dozens of millions of patients suffering from life-threatening neurological diseases," mentioned another researcher.

Researchers find new drug to prevent neural deaths

A team of scientists has found a new drug that may prevent neural death through glucose metabolism modification in stressed neurons.

The trials conducted on mice are rather promising for future use in humans. The new drug can be advantageous in neurological conditions ranging from Amyotrophic lateral sclerosis, Alzheimer's and Huntington's diseases to traumatic brain injury and ischemic stroke.

According to WHO, stroke is the 2nd most common cause of mortality and more than a third of people who have survived a stroke will have a severe disability.

As the population ages, many more millions are poised to develop Alzheimer's or Parkinson's disease in the near future.

Glycolysis is generally considered as the metabolic pathway essential for cell survival since it meets cell energy needs in case of intensive energy consumption.

However, it is already known that in the brain tissue, the situation is quite different-different cell types show distinct glucose metabolism patterns.

In Neurons, only a small portion of glucose is consumed vie the glycolysis pathway. At the same time, astrocytes provide nutrients to neurons and utilise glycolysis to metabolise glucose.

These differences are mostly due to the special protein called PFKFB3, which is normally absent in neurons and is active is astrocytes.

In the case of certain neurological diseases, stroke being one of them, the amount of active PFKFB3 increases in neurons, which is highly stressful for these cells and leads to cell death.
Researchers in the in vivo experiments confirmed that a small molecule, the inhibitor or PFKFB3, may prevent cell death in the case of ischemia injury.

Inhibition of PFKFB3 improves co-ordination of mice after stroke and reduced brain infarct volume. Moreover, PFKFB3 inhibitor protects neurons from the amyloid-beta peptide, the main component of the amyloid plaques found in the brains of Alzheimer's disease patients. 

A Prof. said, " Excitotoxicity is a hallmark of various neurological diseases, stroke being one of them. Our group has previously established a link between this pathological condition and high activity of PFKFB3 enzyme in neurons, which leads to severe oxidative stress and neuronal death".

These promising results bring hope to dozens of millions of patients suffering from life-threatening neurological disease, mentioned a researcher.

THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.                                    PS- THOSE INTERESTED IN RECIPES ARE FREE TO  VIEW MY BLOG-                                                                                           https://gseasyrecipes.blogspot.com/                                                                                                                                                FOR INFO ABOUT KNEE REPLACEMENT, YOU CAN VIEW MY BLOG-                                                                       https:// kneereplacement-stickclub.blogspot.com/                                                                                                                     FOR CROCHET DESIGNS                                                                                                   

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Researchers Look to Old Algae to Combat Alzheimer's

What do algae blooms, British explorers and neurodegenerative diseases have in common? A lot, it turns out.Century-old samples from an Antarctic expedition are helping researchers fighting to find a cure for Alzheimer's and Lou Gehrig's diseases.

Scientists worked with the Natural History Museum in London for over five years to analyze samples of cyanobacteria mats collected in the summer of 1902 by explorer Robert Falcon Scott from ponds and sediment accumulated in the Antarctic.

The samples have been preserved for more than 100 years at the museum in London. After testing them the researchers found the samples contained toxins produced by cyanobacteria, including toxins linked to liver cancer and neurodegenerative diseases.

"We jumped at the chance," one of the researcher said of the collaboration. "We thought, 'Well, we can't lose.' If there are toxins, great. That helps us understand exposure. If not, then it helps with the pollution aspect.

"But it seems like they've always been there and we've always been exposed to them. And it's important for our research to find ways to combat their effects and provide cures for people who may be susceptible to the actions of these toxins," he said.

A Closer Look at Cyanobacteria

This discovery, the result of years of collaboration between scientists, is promising for the future of medicine.

The samples were run through the lab two to three years ago, but the analysis was published recently.

"What drives us is results," he said. "Our only goal is to change patient outcomes."

Alzheimer's is a chronic, progressive neurodegenerative disease that slowly destroys memory and thinking skills. Estimates vary, but experts believe more than 5 million Americans may have Alzheimer's, which is the sixth leading cause of death in the United States.

Amyotrophic lateral sclerosis, also known as Lou Gehrig's disease, is also a progressive neurodegenerative disease. It affects nerve cells in the brain and spinal cord, weakening muscles and affecting physical functions.

The discovery of the toxins in the Antarctic samples provides a much-needed baseline for cyanobacterial toxin levels before pollution and climate change, the scientists say.

"What this shows is that there is a background amount of toxin exposure for people," said one of the scientist. "And we're really interested in how that fits into the puzzle because we know that for certain neurological illnesses, there is a background rate. What this puzzle piece suggests is that we've always been exposed to these toxins as people, as human beings."

The low-level exposure to cyanobacteria could account for a low but constant rate of certain diseases. Recent increases in frequency and duration of cyanobacteria blooms may be associated with increases of neurodegenerative diseases, the scientists believe.

They point to Guam ALS/PDC, a disease that presents traits of ALS and Alzheimer's and Parkinson's diseases. As the name suggests, it is found in people living in Guam.

A cyanobacterial toxin, BMAA, found in contaminated traditional foodstuffs appears to trigger the disease, Cox said. The presence of BMAA has been discovered in the brains of those with the disease but not the brains of the control patients who died of causes unrelated to neurodegeneration.

Confirmation of that pattern was found in replicated experiments, showing that chronic dietary exposure resulted in brain tangles and plaques that were chemically, structurally and positionally identical to the people in Guam with ALS/PDC.

These results that were published recently.

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A single protein may help treat Parkinson’s, Alzheimer’s

Scientists have found that a single protein can lead to effective treatments for devastating neurodegenerative diseases, such as Parkinson's, Huntington’s, Alzeheimer's and amyotrophic lateral sclerosis (ALS). These disorders are triggered by misbehaving proteins in the brain that misfold and accumulate in neurons, inflicting damage and eventually killing the cells. In the study, researchers from the Gladstone Institutes in California, used a different protein — Nrf2 — to restore levels of the disease-causing proteins to a normal, healthy range, thereby preventing cell death. ‘We’ve tested Nrf2 in models of Huntington’s disease, Parkinson’s disease, and ALS, and it is the most protective thing we’ve ever found. Based on the magnitude and the breadth of the effect, we really want to understand Nrf2 and its role in protein regulation better,’ said Steven Finkbeiner from Gladstone Institute. The researchers tested Nrf2 in two models of Parkinson’s disease — cells with mutations in the proteins LRRK2 and alpha-synuclein.

By activating Nrf2, the researchers turned on several ‘house-cleaning’ mechanisms in the cell to remove excess LRRK2 and alpha-synuclein. ‘Nrf2 coordinates a whole program of gene expression, but we didn’t know how important it was for regulating protein levels until now,’ added Gaia Skibinski, research scientist at Gladstone Institute. ‘Over-expressing Nrf2 in cellular models of Parkinson’s disease resulted in a huge effect. In fact, it protects cells against the disease better than anything else we’ve found,’ Skibinski explained. Using a one-of-a-kind robotic microscope, the team tagged and tracked individual neurons — both rat and human — over time to monitor their protein levels and overall health. They took thousands of images of the cells over the course of a week, measuring the development and demise of each one. While, for mutant LRRK2, Nrf2 drove the protein to gather into incidental clumps that can remain in the cell without damaging it, for alpha-synuclein, Nrf2 accelerated the breakdown and clearance of the protein, reducing its levels in the cell, the results showed. The study was published in the Proceedings of the National Academy of Sciences (PNAS). 

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