High salt diet hobbles the brain

A new study has shown that mice fed with a very high-salt diet experienced declined blood flow to their brain, the integrity of blood vessels in the brain suffered, and performance on tests of cognitive function plummeted.

Researchers found that those effects were not as long has been widely believed, a natural consequence of high blood pressure. Instead, they appeared to be the result of signals sent from the gut to the brain by the immune system.

The study, conducted by researchers at Weill Cornell Medicine in New York. The research sheds light on a subject of keen interest to scientists exploring the links between what we eat and how well we think, and the mediating role that the immune system plays in that communication.

This suggests that even before a chronic high-salt diet nudges blood pressure up and compromises the health of tiny blood vessels in the brain, the oversalted gut is independently sending messages that lay the groundwork for corrosion throughout the vital network.

In the small intestines of mice, the authors of the new research found that a very high-salt diet prompted an immune response that boosted circulating levels of an inflammatory substance called interleukin-17. These high levels of IL-17 set off a cascade of chemical responses inside the delicate inner linings of the brain's blood vessels.

The result in mice fed with the high-salt diet: blood supply to two regions crucial for learning and memory-the cortex and hippocampus slowed markedly. And mental performance slid. Compared to mice fed a diet lower in salt, the maze-running skills of the mice who consumed high-salt levels faltered, and they failed to respond normally to whisker stimulation, or a new object in their cage.

In mice, that evidence of cognitive impairment was apparent even in the absence of high blood pressure. The immune system's role in sending signals between brain and gut is also seen in diseases like multiple sclerosis, rheumatoid arthritis, psoriasis and inflammatory bowel disease-all disorders that are linked to poor functioning of the brain's blood vessels.
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Fasting diets boost brain power

Intermittent fasting may provide brain with more energy, improves memory and learning capabilities. When mice were fed every other day, they grew more neurons and synaptic connections, improving their cognitive functions. During intermittent fasting, the body switches energy sources from glucose, made in the liver, to fat cells, which stimulate activity and cell growth in the brain.

The body runs off of the liver's energy stores for about 10 to 14 hours in humans, when those stores are out, human, as well as animal bodies switch to fat stores, which are converted into compounds called ketones in the blood. Ketones act directly on the nerve cells to stimulate production of BDNF'- a key protein to neuron growth-and may help optimize cognition, learning and memory building.

Simply eating less will not have the same effects, eating three meals a day and having an overall relatively low calorie intake - between 1,800 and 2,000 every time-replenish their liver energy stores. The mice in the study were more alert and showed more activity in the areas of their brains responsible for learning and memory during the fasting period. Every-other-day fasting his team used for the mice wouldn't work in human, two days of fasting each week can help in human.
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Transplanted hematopoietic stem cells reverse damage caused by neuro-muscular disorder

Single infusion of wildtype hematopoietic stem and progenitor cells (HSPCs) into a mouse model of Friedreich's ataxia (FA) measurably halted cellular damage caused by the degenerative disease. Friedreich's ataxia is an inherited, degenerative neuromuscular disorder that initially impairs motor function, such as gait and coordination, but can lead to scoliosis, heart disease, vision loss and diabetes. Cognitive function is not affected.

The disease is progressively debilitating, and ultimately requires full-time use of a wheelchair. FA is caused by reduced expression of a mitochondrial protein called frataxin (FXN) due to a two mutated or abnormal copies of the FXN gene. Researchers used a transgenic mouse model that expresses two mutant human FXN transgenes, and exhibits the resulting progressive neurological degeneration and muscle weakness.

Human hematopoietic stem and progenitor cells (HSPCs), derived from bone marrow, have become a primary vehicle for efforts to replace or regenerate cells destroyed by a variety of diseases. Transplanting wildtype or normal mouse HSPCs resulted in long-term kidney, eye and thyroid preservation in a mouse model of cystinosis, another genetic disorder.

Researchers transplanted wildtype HSPCs into an FA mouse model, reporting that the HSPCs engrafted and soon differentiated into macrophages in key regions of the mice's brain and spinal cord where they appeared to transfer wildtype FXN into deficient neurons and muscle cells. Transplantation of wildtype mouse HSPCs essentially rescued FA-impacted cells expression was restored. Mitochondrial function in the brains of the transgenic mice normalized, as did in the heart. There was also decreased skeletal muscle atrophy.
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Green tea may prevent brain impairment

Green tea contains polyphenols, which are antioxidants that are good for overall health. The phytochemicals in green tea prevents neurological disorders like Parkinson’s disease by promoting the production of dopamine.

It can improve cognitive function and may be useful in treating patients who have  brain impairment, Alzheimer’s disease and dementia.

 Regular drinking of green tea extract increased brain activity in the areas of the brain that are responsible for memory function.

Tannins in green tea leaves prevents brain damage that might occur after brain injuries or strokes. Drinking of green tea may combat obesity, insulin resistance and memory impairment.
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