Scientists identify protein that makes women more susceptible to Alzheimer’s

While the accumulation of proteins in the brain is a marker to indicate the onset of Alzheimer's, a new study analysed the ways in which these proteins spread, that might help in describing why the disease is more prevalent in females than males.

A recent study  has identified differences in the spread of a protein called tau, which is linked to cognitive impairment — between men and women, with women showing a larger brain-wide accumulation of tau than men due to an accelerated brain-wide spread.

Accumulating evidence suggests that tau spreads through brain tissue like an infection, traveling from neuron to neuron and turning other proteins into abnormal tangles, subsequently killing brain cells.

Researchers used data from positron emission tomography (PET) scans of healthy individuals and patients with mild cognitive impairment who were enrolled in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database.

“It’s kind of like reconstructing a crime scene after a crime. You weren’t there when it happened, but you can determine where an intruder entered a house and what room they entered next,” said  lead investigator for the study.

“The graph analysis does something similar to show how tau spreads from one region to another,” the investigator added.

The findings showed that the architecture of tau networks is different in men and women, with women having a larger number of “bridging regions” that connect various communities in the brain.

This difference may allow tau to spread more easily between regions, boosting the speed at which it accumulates and putting women at greater risk for developing Alzheimer’s disease.

The lead study investigator said, “Understanding how different biological processes influence our memory is a really important topic.”

“Sex-specific differences in the brain’s pathological, neuroanatomical and functional organization may map into differences at a neurobehavioral and cognitive level, thus explaining differences in the prevalence of neurodegenerative disorders and helping us develop appropriate treatments,” he opined.

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HUMAN BRIAN- ALL YOU WANT TO KNOW ABOUT IT

Human brain if the most interesting and complicated organ. And these facts only prove this statement.

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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.

researchers identify pathway that may protect against cocaine addiction

A study by researchers  gives insight into changes in the reward circuitry of the brain that may provide resistance against cocaine addiction. Scientists found that strengthening signalling along a neural pathway that runs through the nucleus accumbens — a region of the brain involved in motivation, pleasure, and addiction — can reduce cocaine-seeking behaviour in mice.

Research suggests that about 1 in 5 people who use cocaine will become addicted, but it remains unclear why certain people are more vulnerable to drug addiction than others.

A key step in understanding addiction and advancing treatment is to identify the differences in brain connectivity between subjects that compulsively take cocaine and those who do not. 

Until now, most efforts have focused on finding traits associated with vulnerability to develop compulsive cocaine use. However, identifying mechanisms that promote resilience may prove to have more therapeutic value.

In the study, mice were conditioned to receive an intravenous dose of cocaine each time they poked their nose into a hole in their enclosure. Cocaine was then made unavailable for periods of time during the day. Some of the mice would stop seeking the drug once it was removed while others would obsessively continue to poke the hole in an effort to obtain the drug.

Mice that quickly stopped seeking the drug were found to have stronger connections along the indirect pathway — a neural tract that forms indirect projections into the mid-brain and contains cells called medium spiny neurons expressing dopamine D2 receptors (D2-MSNs). A parallel pathway — known as the direct pathway -- forms direct projections into the mid-brain neurons and contains medium spiny neurons expressing D1 receptors (D1-MSNs). These two pathways are thought to work together in complementary but sometimes opposing ways to affect behaviour.

Researchers were very surprised by the results of the study because we were originally looking for vulnerability factors for developing compulsive drug use. Instead,they found changes that only happened in subjects that show a resilience to becoming compulsive drug users. Resilient mice had a strong inhibitory circuit that allowed them to exert better control over their drug intake.

To test this observation, researchers used lasers to activate individual neurons, and found that stimulating D2-MSNs in the nucleus accumbens decreased cocaine seeking in the mice. Blocking D2-MSN signalling with a chemical process increased motivation to obtain cocaine.

This research advances the understanding of how the recruitment, activation and the interaction among brain circuits can either restrain or increase motivation to take drugs.

Previous studies have shown that people with lower levels of dopamine D2 receptors in the striatum, a brain region associated with reward and working memory, are more likely to develop compulsive behaviours toward stimulant drugs.

Dopamine is a key neurotransmitter involved in reward-based learning and addiction. Cocaine disrupts communication between neurons at the synapse, the small junction between nerve cells, by blocking the re-absorption of dopamine into the transmitting neuron. As a result, dopamine continues to stimulate the receiving neuron, causing feelings of alertness and euphoria.

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.