Eating More Mushrooms Could Improve Your Mental Health

Mushrooms are  delicious and versatile, and many of our favorite recipes call for everything from tender chanterelles to chopped creminis. But their flavor isn't the only reason why you should pack your diet with mushrooms: A study has discovered that a compound found in all mushrooms could be used to prevent cognitive decline as we age.

Degenerating mental health is often referred to as mild cognitive impairment, or MCI, by medical professionals. Those suffering from MCI are normally able to live independently, but they could have difficulty understanding routine tasks or processing everyday information. According to the doctors , more than six percent of those in their 60s experience MCI, whereas 37 percent of those over 85 are suffering this mild form of cognitive decline.

New research  pinpoints measures that could reduce those statistics. More than 600 seniors living in Singapore participated in a six-year study that measured how many mushrooms they consumed on a daily basis—these participants were divided into groups based on the varying amounts of fresh mushrooms they ate. The groups that consumed more than two servings of mushrooms per day were found to have 50 percent less cases of MCI than the seniors who ate less.

One serving was defined as 3/4 of a cup of cooked mushrooms ; researchers tested multiple varieties in the study, including shiitake, oyster, golden, and white button mushrooms. They came to the conclusion that any variety of mushroom would have produced similar results.

How did they measure mental health? Each participant was asked to complete an interview that included a common IQ test known as the Wechsler Adult Intelligence Scale. "The interview takes into account demographic information, medical history, psychological factors, and dietary habits," The study's lead author, told  "A nurse will measure blood pressure, weight, height, handgrip, and walking speed. They will also do a simple screen test on cognition, depression, anxiety."

Researchers pinpointed high concentrations of ergothioneine as the protective agent that boosts mental health—since ergothioneine is an antioxidant, the compound could also help reduce inflammation in the body. Furthermore, mushrooms contain high amounts of other compounds (erinacines, scabronines, and hericenones) that could prevent cognitive decline by aiding nerve growth in the brain and preventing production of beta amyloid, which has previously been linked to dementia.

Scientists are planning additional experiments to further test their findings. A new randomized controlled trial is now underway, where participants will be given pure ergothioneine along with other plant compounds to confirm mushrooms' holistic health boost.

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/    

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Blood Pressure, Diabetes and Smoking Problems During Middle Age May Lead to Dementia Later

Middle-aged people with diabetes and high blood pressure beware. According to a latest study, those in their 40's and 50's who have cardiovascular health risk factors, and are also regular smokers, are at a higher risk of suffering from dementia in later in life. According to the findings, the chances of dementia increased significantly, with age due to the presence of APOE4 - a gene associated with Alzheimer's disease.

A Professor said, "Diabetes or high blood pressure, also called hypertension, increased the chances of developing dementia. Importantly, diabetes was found to be almost as strong a predictor of dementia as the presence of the APOE4 gene. Our results contribute to a growing body of evidence linking midlife vascular health to dementia."

"These are modifiable risk factors. Our hope is that by addressing these types of factors early, people can reduce the chances that they will suffer from dementia later in life," Prof. added.

The researchers also went on to find a link between dementia and pre-hypertension, which is a condition in which blood pressure levels are higher than normal but lower than hypertension. The study is alarming as the researchers claimed that diabetes, hypertension and pre-hypertension increased the chances of dementia for all participants. In addition the study stated that smoking cigarettes may also play a role in increasing the chances of dementia.

For the study, the team analyzed the data of 15,744 persons, from 1987-1989 aged 45-64 years. During an average of 23 follow-up years, the team found 1,516 participants to be diagnosed with dementia.

In a separate study, the Prof. also discovered that the presence of one or more vascular risk factors during midlife could be linked with higher levels of beta amyloid - a protein that often accumulates in the brains of Alzheimer's patients. The researchers noted that this relationship was not affected by the presence of the APOE4 gene and not seen for risk factors which could present themselves in later life.

Dr. says "According to Ayurveda, consuming garlic cloves and gooseberries can work wonders for high blood pressure patients."

Here's how these Ayurvedic recommendations  can come in handy to keep your Blood pressure in control.

According to Ayurvedic Remedies, these food and herbs can help fight high blood pressure -
1.Cardamom
A teaspoon coriander and one pinch of cardamom to one cup of freshly squeezed peach juice can help bring down high blood pressure.

2.Cucumber
Consuming some cucumber raita can help too, Cucumber is a good diuretic, which helps reducing hypertension.

3.Honey
Add a teaspoon of honey and 5 to 10 drops of apple cider vinegar to a cup of hot water and consume it early morning. It helps reduce and regulate blood pressure.

4.Herbal concoction of herb 'Punarnava'
A mixture of Punarnava (1 part), passion flower(1 part) and hawthorn berry(2 parts) can also go a long way in controlling hypertension. Steep half a teaspoon of the mixture in a cup of hot water for 5 to 10 minutes and drink the tea after lunch and dinner.

5.Ashwagandha
Ashwagandha in conjunction with other herbs like Gotu Kola may also prove to be an effective formula to control hypertension, according to Ayurveda.

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High blood-sugar makes Alzheimer's more deadly

A new study has revealed that high blood-sugar levels, such as those linked with Type 2 

diabetes, make beta amyloid protein associated with Alzheimer's disease dramatically 

more toxic to cells lining blood vessels in the brain.

The  study supports growing evidence pointing to glucose levels and vascular damage as 

contributors to dementia.

"Previously, it was believed that Alzheimer's disease was due to the accumulation of 

'tangles' in neurons in the brain from overproduction and reduced removal of beta amyloid 

protein," senior investigator said.

"While neuronal involvement is a major factor in Alzheimer's development, recent 

evidence indicates damaged cerebral blood vessels compromised by high blood sugar 

play a role. Even though the links among Type 2 diabetes, brain blood vessels and 

Alzheimer's progression are unclear, hyperglycemia appears to play a role," he said.

ps- this is only for information, always consult you physician before having any particular food/ medication/exercise/other remedies.

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Suppressing protein may stem Alzheimer's disease process

Scientists  have discovered a potential strategy for developing treatments to stem the disease process in Alzheimer's disease. It’s based on unclogging removal of toxic debris that accumulates in patients’ brains, by blocking activity of a little-known regulator protein called CD33.

Too much CD33 appears to promote late-onset Alzheimer's by preventing support cells from clearing out toxic plaques, key risk factors for the disease . Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.

Variation in the CD33 gene turned up as one of four prime suspects in the largest genome-wide dragnet of Alzheimer's affected families. The gene was known to make a protein that regulates the immune system, but its function in the brain remained elusive. To discover how it might contribute to Alzheimer's  the researchers brought to bear human genetics, biochemistry and human brain tissue, mouse and cell-based experiments.

They found over-expression of CD33 in support cells, called microglia, in post-mortem brains from patients who had late-onset Alzheimer's disease, the most common form of the illness. The more CD33 protein on the cell surface of microglia, the more beta-amyloid proteins and plaques — damaging debris — had accumulated in their brains. Moreover, the researchers discovered that brains of people who inherited a version of the CD33 gene that protected them from Alzheimer's conspicuously showed reduced amounts of CD33 on the surface of microglia and less beta-amyloid.

Brain levels of beta-amyloid and plaques were also markedly reduced in mice engineered to under-express or lack CD33. Microglia cells in these animals were more efficient at clearing out the debris, which the researchers traced to levels of CD33 on the cell surface.

Evidence also suggested that CD33 works in league with another Alzheimer's risk gene in microglia to regulate inflammation in the brain.

The study results — and those of a recent rat study that replicated many features of the human illness — add support to the prevailing theory that accumulation of beta-amyloid plaques are hallmarks of Alzheimer's pathology. They come at a time of ferment in the field, spurred by other recent contradictory evidence  suggesting that these presumed culprits might instead play a protective role.

Since increased CD33 activity in microglia impaired beta-amyloid clearance in late onset Alzheimer’s, researchers are now searching for agents that can cross the blood-brain barrier and block it.

Activity of a regulator protein called CD33 (green) clogs removal of brain-damaging debris, beta-amyloid protein (red), by support cells, microglia. Left: Microglia of normal control mice (A”) show more CD33 and less beta-amyloid than mice in which CD33 expression is experimentally knocked-out (B”). Right: Little beta-amyloid can be seen in microglia of a mouse line in which CD33 is over-expressed (C”), compared to microglia of mice in which CD33 is experimentally inactivated (D”). Evidence from post-mortem human brains indicates that CD33 is similarly overactive in Alzheimer’s disease, suggesting that a treatment that impedes it might help treat or prevent the disease. Source:Rudolph Tanzi, Ph.D. , of Massachusetts General Hospital and Harvard University

Contagion

Alzheimer’s disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau.

The surprising finding answers a longstanding question and has immediate implications for developing treatments, researchers said. And they suspect that other degenerative brain diseases like Parkinson’s may spread in a similar way.

Alzheimer’s researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas that involve remembering and reasoning.

But for more than a quarter-century, researchers have been unable to decide between two explanations. One is that the spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths that nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and resist the disease longer.

The new studies provide an answer. And they indicate it may be possible to bring Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau.

The studies, done independently by researchers at Columbia and Harvard, involved genetically engineered mice that could make abnormal human tau proteins, predominantly in the entorhinal cortex, a sliver of tissue behind the ears, toward the middle of the brain, where cells first start dying in Alzheimer’s disease. As expected, tau showed up there. And, as also expected, entorhinal cortex cells in the mice started dying, filled with tangled, spaghettilike strands of tau.

Over the next two years, the cell death and destruction spread outward to other cells along the same network. Since those other cells could not make human tau, the only way they could get the protein was by transmission from nerve cell to nerve cell.

Although the studies were in mice, researchers say they expect that the same phenomenon occurs in humans because the mice had a human tau gene and the progressive wave of cell death matched what they see in people with Alzheimer’s disease.

Two groups of researchers were inspired by the many observations over the years that Alzheimer’s starts in the entorhinal cortex and spreads.

Researchers knew that something set off Alzheimer’s disease. The most likely candidate is a protein known as beta amyloid, which accumulates in the brain of Alzheimer’s patients, forming hard, barnaclelike plaques. But beta amyloid is very different from tau. It is secreted and clumps outside cells. Although researchers have looked, they have never seen evidence that amyloid spreads from cell to cell in a network.

Still, amyloid creates what amounts to a bad neighbourhood in memory regions of the brain. Then tau comes in — some call it “the executioner” — piling up inside cells and killing them. If some cells take longer than others to succumb to the bad neighbourhood, that would explain the spread of the disease in the brain, and there would be no need to blame something odd, like the spread of tau from cell to cell.

The question of which hypothesis was correct — tau spreading cell to cell, or a bad neighbourhood in the brain and cells with different vulnerabilities to it — remained unanswerable. A Dr  said he tried for 25 years to find a good way to address it. One of his ideas was to find a patient or two who had had a stroke or other injury that severed the entorhinal cortex from the rest of the brain. If the patient developed Alzheimer’s in the entorhinal cortex — and it remained contained there — he would have evidence that the disease spread like an infection.

The solution came when researchers were able to develop genetically engineered mice that expressed abnormal human tau, but only in their entorhinal cortexes. Those mice offered the cleanest way to get an answer, said John Hardy, an Alzheimer's researcher at University College London who was not involved in either of the new studies.

There is another advantage, too,  the Dr  said. The mice give him a tool to test ways to block tau’s spread — and that, he added, “is one of the things we’re excited about.”

But if tau spreads from neuron to neuron,  it may be necessary to block both beta amyloid production, which seems to get the disease going, and the spread of tau, which continues it, to bring Alzheimer’s to a halt. He and others are also asking if other degenerative diseases spread through the brain because proteins pass from nerve cell to nerve cell.

Distorted protein

Alzheimer’s researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas that involve remembering and reasoning.

But for more than a quarter-century, researchers have been unable to decide between two explanations. One explanation is that the spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths that nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and resist the disease longer.

The new studies provide an answer. And they indicate it may be possible to bring Alzheimer's disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau.