Depression linked to brain inflammation

Years of depression can cause brain inflammation that has been linked to degenerative diseases like Alzheimer's and Parkinson's, an analysis of brain-changes among people whose depression lasted more than 10 years, done by the Canadian Centre for Addiction and Mental Health, suggested doctors may need to treat both depression and inflammation in these patients.

The average, untreated bout of depression typically lasts a few months, according to Harvard University. Everyone's symptoms vary in type, severity, and duration. Depression may look like irritability or simply a 'low mood.' But the staying power of depression may make it even more difficult to diagnose, as years of the disorder come to be seen as 'normal' for the person suffering the symptoms.

This may be why the average age of diagnosis for persistent depressive disorder (PDD) is relatively late, at 31 years old. The condition is also known to affect eating habits and experiences. Some tend to overeat when they are depressed, others lose their appetites, and still others will experience upset stomachs.

A high number of physical complaints may also be, in some cases, a warning sign that someone is depressed or in the throes of another mental health issue. Depression typically involves a shortage of serotonin, a neurochemical that nerve cells use to communicate a command for blood vessels to constrict. This is particularly important to the way that the digestive tract functions, as well as to the experience of pain.

Depression is a physical illness that could be treated with anti-inflammatory drugs, an overactive immune system may trigger the mental health condition by causing widespread inflammation that leads to feelings of hopelessness and unhappiness. The immune system may fail to 'switch off' after an illness or traumatic event. Previous research has shown people who suffer severe emotional trauma have signs of inflammation, which suggests their immune system is constantly 'fired-up'.

Researchers from the Center for Addiction and Mental Health (CAMH) found evidence that longer bouts of depression increased brain inflammation. To determine whether or not the duration of depression made a difference for its inflammatory effects, the research team, led by senior study author Dr Jeff Meyer of CAMH's Campbell Family Mental Health Research Institute recruited three groups of 25 people.

The first group had experienced more than a decade of depression, the second had experienced less than a decade, and the third had never experienced any depression, by their own reports. The difference between the PDD sufferers and the other two groups was dramatic. Those who had been depressed for more than 10 years had 30 percent more of a protein marker of brain-inflammation than those who had experienced depression, but for shorter amounts of time.

Their inflammation levels were also higher than the control group that had never been depressed. Greater inflammation in the brain is a common response with degenerative brain diseases as they progress, such as with Alzheimer's disease and Parkinson´s diseases.
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Traumatic brain injury causes intestinal damage

Researchers has found a two-way link between traumatic brain injury (TBI) and intestinal changes. These interactions may contribute to increased infections and may worsen chronic brain damage. This is the first study to find that TBI in mice can trigger delayed, long-term changes in the colon and that subsequent bacterial infections in the gastrointestinal system can increase post traumatic brain inflammation and associated tissue loss.

These results indicate strong two-way interactions between the brain and the gut that may help explain the increased incidence of systemic infections after brain trauma and allow new treatment approaches. TBI has significant effects on the gastrointestinal tract, brain trauma can make the colon more permeable, potentially allowing harmful microbes to migrate from the intestine to other areas of the body, causing infection.

People are 12 times more likely to die from blood poisoning after TBI, which is often caused by bacteria, and 2.5 times more likely to die of a digestive system problem, compared with those without such injury.In this study, the researchers examined mice that received an experimental TBI. They found that the intestinal wall of the colon became more permeable after trauma. It is not clear how TBI causes these gut changes.

A key factor in the process may be enteric glial cells (EGCs), a class of cells that exist in the gut. These cells are similar to brain astroglial cells, and both types of glial cells are activated after TBI. After TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain. Researchers don't know whether activation of ECGs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.

The researchers also focused on the two-way nature of the process: how gut dysfunction may worsen brain inflammation and tissue loss after TBI. They infected the mice with Citrobacter rodentium, a species of bacteria that is the rodent equivalent of E. coli, which infects humans. In mice with a TBI who were infected with the bacteria, brain inflammation worsened.

Furthermore, in the hippocampus, a key region for memory, the mice who had TBI and were then infected lost more neurons than animals without infection. This suggests that TBI may trigger a vicious cycle, in which brain injury causes gut dysfunction, which then has the potential to worsen the original brain injury.
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Risk factors for Marburg infections

People at risk of Marburg infection are those who come in contact with African monkeys and bats, researchers on these viruses are also at higher risk of becoming infected, African miners due to their exposure to bats. Veterinarians may also be at higher risk if they are exposed to African monkeys. Also, people who care for Marburg virus-infected patients and health workers who remove those bodies of deceased Marburg virus-infected patients are at high risk of contracting the disease.

Patients are given supportive hospital care by maintaining their fluid and electrolyte balance and other considerations, such as replacing lost blood and maintaining a good oxygen supply. This supportive care is most effectively done in an intensive-care hospital unit. Most individuals with Marburg virus infections are treated in hospitals in the intensive-care units. Specialists who treat the patient are critical-care specialists, hematologists, infectious-disease specialists, hospitalists, and lung specialists.

There is no antiviral drug or vaccine approved for use in humans against Marburg viruses. Preventive measures are based on barrier techniques (isolation techniques) that isolate the infected patient from other humans. Those health-care professionals who treat Marburg virus-infected patients must use barrier protections such as gowns, gloves, masks, and shoe coverings.

The prognosis for Marburg infection ranges from fair to poor. The fatality rate varies from about 23%-90%. Individuals cared for in an intensive-care unit have a better chance of survival. Complications that can occur with Marburg infection include the following: inflammation of the retinas of the eyes, inflammation of the testes,
liver inflammation, inflammation within the pigmented layer of the eye, inflammation of a segment of the spinal cord and brain inflammation.

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Meningococcal B vaccine may prevents gonorrhoea

Vaccine used against a bacteria that causes brain inflammation can prevents gonorrhoea. Presently, using a condom or abstaining from sex are ways of preventing gonorrhoea.

Gonorrhoea can cause painful pelvic inflammation in women, and infertility in men and women. It can also spread into the bloodstream to cause life-threatening infections in other parts of the body. Infected pregnant woman can pass it to her fetus and cause blindness.

The disease spreads easily because many carriers are unaware of the disease, until they experience the symptoms. Gonorrhoea is becoming untreatable because of antibiotic resistance, there is an increased imperative to examine different vaccine for the treatment.

Researchers examined gonorrhoea cases among people who have used meningococcal B vaccine for Meningococcal bacteria, they noticed a decline in gonorrhoea after the use of meningococcal B vaccine.
This shows that meningitis vaccine can prevents gonorrhoea.
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