BP drug shows promise for treating Parkinson's

Felodipine, a prescribed drug to treat high blood pressure, has shown promise against Parkinson's, Huntington's and forms of dementia in studies carried out in mice and zebra-fish.

In a study, scientists have shown in mice that felodipine may be a candidate for re-purposing.

A common feature of neuro-degenerative diseases is the build-up of misfolded proteins.

These proteins, such as huntingtin in Huntington's disease and tau in some dementias, form "aggregates" that can cause irreversible damage to nerve cells in the brain.

A team led by a Prof. used mice that had been genetically modified to express mutations that cause Huntington's disease or a form of Parkinson's disease, and zebra-fish that model a form of dementia.

Felodipine was effective at reducing the build-up of "aggregates" in mice with the Huntington's and Parkinson's disease mutations and in the zebrafish dementia model.

The treated animals also showed fewer signs of diseases.

"This is the first time that we're aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans," said the Prof.

The hypertension drug was able to slow down the progression of these potentially devastating conditions and "so we believe it should be trialed in patients," he added.

In healthy individuals, the body uses a mechanism to prevent the build-up of such toxic materials.
This mechanism is known as autophagy, or 'self-eating', and involves cells eating and breaking down the materials.

"This is only the first stage, though. The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. We need to be cautious, but I would like to say we can be cautiously optimistic," said the Prof. 

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Scientists May Have Found the Cause of Alzheimer’s Disease—and How to Reverse It

The tragedy of Alzheimer’s disease begins with the way it robs memory, personality, and lives. Then there’s the condition’s resistance to treatment: 99 percent of the therapies developed by neurologists and pharmaceutical companies have failed, according to a recent study. There may be hope on the horizon, though. Two new areas of research suggest that the disease may be a type of infection—and we may already have a way to treat it.

For decades, brain researchers have focused on blocking one of the earliest signs of Alzheimer’s—the buildup of proteins known as amyloid and tau. Scientists have designed many therapies that target the plaques and tangles left by amyloid and tau, but in test after test, patients fail to benefit. Recently, experts have begun to doubt the “amyloid hypothesis” as a cause of Alzheimer’s in part because blocking the proteins doesn’t seem to do any good, but also because many people have amyloid plaques but no symptoms of Alzheimer’s.

A new theory has emerged, and it not only explains why patients can have masses of amyloid and tau proteins in the brain, but also why targeting those proteins won’t help: Welcome to the “infection hypothesis.” Brain scientists have learned that these proteins act as part of the brain’s defense system, trapping infectious invaders like bacteria and viruses. In other words, rather than amyloid and tau being the cause of Alzheimer’s disease, they could be a symptom. If a lot of microbial invaders make it passed the blood-brain barrier and take up residence, the brain could end up with loads of plaque and tangles.

This is where the new studies—and the infectious hypothesis—comes in. A team of researchers have found that the bacteria behind chronic gum disease, Porphyromonas gingivalis, can migrate to the brain. Once there, the bacteria releases toxins called gingipains that attack the areas of the brain involved in memory and critical thinking. Some studies have found that living with gingivitis (gum disease) for more than 10 years increases the risk of Alzheimer’s by as much as 70 percent, according to reports. 

In a study, the team analyzed the brains of deceased Alzheimer’s patients as well as living ones suspected of having the condition; sure enough, the bacteria was present and seemed to contribute to disease progression. Their findings are the first to establish a link between the P. gingivalis and Alzheimer’s in humans, according to a resercher. It also suggests the “potential for a class of molecule therapies” in the treatment of the disease, though more study needs to be done, he cautions.

There may be more than one type of brain intruder responsible for Alzheimer’s. A review of research  published  points to evidence dating back to 1991 that herpes simplex virus 1 (HSV-1—it causes cold sores) can be linked to Alzheimer’s. The trick has been determining whether it’s there by coincidence or if it’s actively damaging the brain—something a study published earlier this year in Neurotherapeutics helped tease out. Taiwanese epidemiologists discovered that people infected with HSV-1 had three times the risk of developing Alzheimer’s later in life compared with those who were virus-free. Even more remarkable, the researchers found that infected patients who had sought antiviral treatment (using drugs like acyclovir) were able to cut their risk of Alzheimer’s by a factor of ten. In  a commentary on the study, experts  say that the results raise the possibility that antiviral drugs—and potentially vaccinations—may offer protection against Alzheimer’s. Here are some other diseases some scientists think may be related to Alzheimer's.

These results are giving researchers the hope that they’re honing in on a potential source—and solution—for Alzheimer’s. The reality is that there may be numerous microbes that can infect the brain: A recent finding indicates a strong connection between Alzheimer’s and the herpes viruses (HSV-6A and HSV-7) responsible for the childhood rash called roseola. Another possible key to the puzzle is that having a genetic susceptibility to Alzheimer’s—a variant of the ApoE gene—seems to leave people more vulnerable to the ravages of these viruses and bacteria. 

Last year, the National Institutes of Health spent almost $2 billion on researching the amyloid hypothesis. Recently, the Infectious Diseases Society of America announced $100,000 in grants for researchers exploring the infectious hypothesis, reports NPR. It’s a drop in the bucket by comparison, but new infectious-related studies are already underway, testing antiviral drugs, vaccines, and even medications that can block damaging gingipain toxins. While it might sound bizarre and frightening that you could “catch” Alzheimer’s disease, the infectious hypothesis could become a welcome reality. 

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Poor sleep may predict Alzheimer's risk in elderly

Poor sleep quality may signal the risk of Alzheimer's disease in older adults, a study suggests.
People with Alzheimer's tend to wake up tired and their nights become even less refreshing as memory loss and other symptoms worsen. 

However, the reason was not fully understood.

The study found that older adults who sleep poorly or have less slow-wave sleep -- deep sleep needed to consolidate memories and wake up feeling refreshed -- have higher levels of tau -- a toxic brain protein.

Tau has also been linked to brain damage and cognitive decline.

"Measuring how people sleep may be a non-invasive way to screen for Alzheimer's disease before or just as people begin to develop problems with memory and thinking," said lead author.

Moreover, the findings, showed that it was not the total amount of sleep that was linked to tau, but the slow-wave sleep, which reflects quality of sleep. 

The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren't getting as good quality sleep.

"What's interesting is that we saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired, meaning that reduced slow-wave activity may be a marker for the transition between normal and impaired," the author added.

For the study, the team studied 119 people aged 60 or older among which almost 80 per cent were cognitively normal and the remainder were very mildly impaired.

Up to two decades before Alzheimer's symptoms of memory loss and confusion appear, amyloid beta protein begins to collect into plaques in the brain. Tangles of tau appear later, followed by decline of key brain areas. Only then do people start showing unmistakable signs of cognitive decline.

The challenge is finding people on track to develop Alzheimer's before such brain changes undermine their ability to think clearly. For that, sleep may be a handy marker, the researchers said.

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'Stress protein' speeds progression of Alzheimer's

A stress-related protein genetically linked to depression, anxiety and other psychiatric disorders contributes to the acceleration of Alzheimer's disease, a new study has found.

Researchers  found when the stress-related protein FKBP51 partners with another protein known as Hsp90 it prevents the clearance from the brain of the toxic tau protein associated with Alzheimer's disease.

Under normal circumstances, tau helps make up the skeleton of our brain cells.

The study was done using test tube experiments, mice genetically engineered to produce abnormal tau protein like that accumulated in the brains of people with Alzheimer's disease, and post-mortem human Alzheimer's brain tissue.

The researchers reported that FKBP51 levels increase with age in the brain, and then the stress-related protein partners with Hsp90 to make tau more deadly to the brain cells involved in memory formation.

Hsp90 is a chaperone protein, which supervises the activity of tau inside nerve cells. Chaperone proteins typically help ensure that tau proteins are properly folded to maintain the healthy structure of nerve cells.

However, as FKBP51 levels rise with age, they usurp Hsp90's beneficial effect to promote tau toxicity.

"We found that FKB51 commandeers Hsp90 to create an environment that prevents the removal of tau and makes it more toxic," said the study's principal investigator .

"Basically, it uses Hsp90 to produce and preserve the bad tau," he said.

The researchers concluded that developing drugs or other ways to reduce FKB51 or block its interaction with Hsp90 may be highly effective in treating the tau pathology featured in Alzheimer's disease, Parkinson's disease dementia and several other disorders associated with memory loss.

A previous study by them found that a lack of FKBP51 in old mice improved resilience to depressive behaviour.

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Cinnamon may prevent Alzheimer's according to a study.

The common baking spice cinnamon may hold the key to delaying the onset of - or warding off - the effects of Alzheimer's disease, scientists have found.

Scientists  found that two compounds in cinnamon - cinnamaldehyde and epicatechin - show some promise in the effort to fight the disease.

According to them, the compounds have been shown to prevent the development of the filamentous "tangles" found in the brain cells that characterise Alzheimer's.

Responsible for the assembly of micro-tubules in a cell, a protein called tau plays a large role in the structure of the neurons, as well as their function.

"The problem with tau in Alzheimer's is that it starts aggregating," said  a researcher.

When for the protein does not bind properly to the microtubules that form the cell's structure, it has a tendency to clump together, she explained, forming insoluble fibres in the neuron.

The older we get the more susceptible we are to these twists and tangles, Alzheimer's patients develop them more often and in larger amounts.

The use of cinnamaldehyde, the compound responsible for the bright, sweet smell of cinnamon, has proven effective in preventing the tau knots.

By protecting tau from oxidative stress, the compound, an oil, could inhibit the protein's aggregation. To do this, cinnamaldehyde binds to two residues of an amino acid called cysteine on the tau protein.

The cysteine residues are vulnerable to modifications, a factor that contributes to the development of Alzheimer's.
Previous research indicates that there is a high correlation between Type 2 diabetes and the incidence of Alzheimer's disease.
The elevated glucose levels typical of diabetes lead to the overproduction of reactive oxygen species, resulting in oxidative stress, which is a common factor in both diabetes and Alzheimer's disease.

Other research has shown cinnamon's beneficial effects in managing blood glucose and other problems associated with diabetes.

"Since tau is vulnerable to oxidative stress, this study then asks whether Alzheimer's disease could benefit from cinnamon, especially looking at the potential of small compounds," said a researcher.

Although this research shows promise, a researcher said, they are "still a long way from knowing whether this will work in human beings."

The researchers caution against ingesting more than the typical amounts of cinnamon already used in cooking.

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.