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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Effects of estrogen treatment in multiple sclerosis

A study by UCLA researchers reveals the cellular basis for how the hormone estrogen protects against damage to the central nervous system in people with multiple sclerosis (MS). The researchers found that estrogen treatment exerts positive effects on two types of cells during disease -immune cells in the brain and also cells called oligodendrocytes. Complementary actions on these two types provide protection from disease.

Multiple sclerosis is a chronic autoimmune, neurodegenerative disease marked by visual impairment, weakness and sensory loss, as well as cognitive decline. These symptoms emerge when inflammatory immune cells destroy the myelin sheath that surrounds nerve processes called axons. Loss of that protective insulation disrupts electrical communication between nerve cells. The third trimester of pregnancy has been previously shown to reduce relapse rates by approximately 70 percent as compared to before pregnancy, and other studies have shown benefit over the long term due to multiple pregnancies.

An estrogen unique to pregnancy that is made by the fetus and placenta has been proposed by Dr. Rhonda Voskuhl and colleagues to mediate this pregnancy protection in both the MS mouse model as well as in two successfully completed clinical trials of estriol treatment in MS patients. How that happens has remained a critical question. Voskuhl, who led the latest study, reported mouse studies showing that estrogen protected the brain from damage by activating a protein called estrogen receptor beta (ERb). Her new research identifies which cells within the brain are mediating this protective effect.

The researchers first genetically eliminated ERb in either immune cells of the brain or in oligodendrocytes, the cells that make the myelin sheath, as a way of making cells unresponsive to estrogen during the MS like disease in mice. They then treated mice without or with ERb in these cells to ask if disease protection was lost or not. Loss of protection during treatment meant that the treatment was acting on the cell that had the receptor removed. Results showed that the estrogen-like treatment was acting on both immune cells of the brain as well as on oligodendrocytes, together resulting in repair of myelin and less disability.

Drug developers often optimize therapies by targeting only one single cell type. By contrast, this study confirms that this estrogen-like compound can combat MS via complementary effects on two distinct cell types. Voskuhl and other UCLA researchers are in fact now developing a next-generation estrogen-like compound with robust biochemical effects on oligodendrocytes and immune cells in the brain.
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Urea in the brain causes dementia

 The build-up of urea in the brain to toxic levels can cause brain damage - and eventually dementia. Metabolic linkages between Huntington's, other neurodegenerative diseases and type-2 diabetes. Huntington's Disease - one of seven major types of age-related dementia - is directly linked to brain urea levels and metabolic processes. Urea is similarly linked to Alzheimer's disease.

The Huntington's study also showed that the high urea levels occurred before dementia sets in, which could help doctors to one day diagnose and even treat dementia, well in advance of its onset. Urea and ammonia in the brain are metabolic breakdown products of protein. Urea is more commonly known as a compound which is excreted from the body in urine. If urea and ammonia build up in the body because the kidneys are unable to eliminate them, for example, serious symptoms can result.

Alzheimer's and Huntington's are at opposite ends of the dementia spectrum. Dementia results in a progressive and irreversible loss of nerve cells and brain functioning, causing loss of memory and cognitive impairments affecting the ability to learn. Currently, there is no cure.

The team used human brains, donated by families for medical research, using cutting-edge gas chromatography mass spectrometry to measure brain urea levels. For levels to be toxic urea must rise 4-fold or higher than in the normal brain. Treating this metabolic state in the brain may help in the regeneration of tissue that can reverse dementia.
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Using silk to repair spinal cord

Modified silk from Asian wild silkworms could be used in a strategy to repair damaged spinal cords, according to scientists. Cleaned, sterilised silk from the Antheraea pernyi (AP) silk spinner had properties well suited to spinal repair.

Presently there is no cure for serious spinal cord trauma because spinal nerves are unable to cross the scar tissue barrier and the cavity that forms in the cord after the injury. The modified silk would be a 'scaffold' that bridges the spinal injury cavity, supporting nerve growth across damaged region.

Modified silk from Asian wild silkworms could be used in a strategy to repair damaged spinal cords, according to scientists. Cleaned, sterilised silk from the Antheraea pernyi (AP) silk spinner had properties well suited to spinal repair.


Scientists discovered that the modified AP silk had important properties desirable in a scaffold suitable for spinal repair. It has the correct rigidity: if it is too rigid it can harm the surrounding spinal cord tissue but if it is too soft the nerves would fail to grow across it.

The AP silk has a repeated "RGD" chemical sequence on its surface that binds to receptors on the nerve cells, encouraging them to attach to the material and grow along it. The AP silk did not trigger a response by the immune system cells that would be present in the spinal cord, therefore minimising inflammation.

AP silk degrades gradually over time. So, after it has supported the early growth of nerves across the injury site the material dissolves gradually and these pioneer nerves take over the role as scaffold, supporting further nerve growth.

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Immune and nerve cells fight gut infections

Nerve cells in the gut play a crucial role in the body's ability to produce an immune response to infection. The immune system and nervous system worked together to respond to infectious threats.

The immune system and neuronal system don't act independently,
The lining of the gut house many immune system cells, which serve as a defense against parasites and other infections.

It is also loaded with nerve cells, immune system cells in the gut, called group 2 innate lymphoid cells (ILC2s), are intertwined with nerve cells called cholinergic neurons.

The ILC2 cells have a receptor for a protein called neuromedin U (NMU), which acts as a messenger for the nerve cells. Exposing ILC2 cells to NMU causes the ILC2 cells to multiply rapidly and secrete chemicals called cytokines that may help trigger an immune response or cause inflammation.

Administering NMU to mice infected with a gut parasite triggered inflammation and a powerful
immune response that expel the parasites quickly.

This shows that the NMU-producing nerve cells help the ILC2 cells, enabling them to rapidly and effectively respond to infection. The findings may improve fighting and provision of therapies for inflammatory diseases like asthma, food allergies and inflammatory bowel diseases.
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Tissues nanotransfection device

Researchers have developed a new technology called Tissue Nanotransfection TNT, it can generate any cell type for treatment within the patient's body. This technology can be used to repair injured tissue or restore function of aging tissue like organs, blood vessels and nerve cells.

Researchers reprogram skin cells to become vascular cells in injured legs that lacked blood flow. Within one week, active blood vessels appeared in the injured leg, the leg was healed at the second week.

The technology also reprogram skin cells in the live body into nerve cells that were injected into brain-injured mice to help them recover from stroke.
The device delivers new DNA or RNA into living skin cells to change their function.

This technology can convert skin cells into elements of any organ with a touch. It takes less than a second and is non-invasive. The chip does not stay permanently in the body after use and the technology keeps the cells in the body under immune surveillance.

TNT technology has two major components: nanotechnology-based chip designed to deliver cargo to adult cells in the live body and the design of specific biological cargo for cell conversion.

 This cargo converts an adult cell from one type to another. TNT doesn't require any laboratory-based procedures and may be implemented at the point of care.
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Cannabis reverses aging brain

Memory performance decreases with increasing age. Cannabis can reverse these ageing processes in the brain. This was shown in mice by scientists at the University of Bonn with their colleagues at The Hebrew University of Jerusalem (Israel).

Old animals were able to regress to the state of two-month-old mice with a prolonged low-dose treatment with a cannabis active ingredient. This opens up new options, for instance, when it comes to treating dementia.

Cognitive ability also decreases with increasing age. This can be noticed, for instance, it becomes more difficult to learn new things or devote attention to several things at the same time and this can leads to dementia.

Researchers have long been looking for ways to slow down or even reverse this process. Scientists at the University of Bonn and The Hebrew University of Jerusalem (Israel) have now achieved this in mice. These animals have a relatively short life expectancy in nature and display pronounced cognitive deficits even at twelve months of age.

The researchers administered a small quantity of THC, the active ingredient in cannabis, to mice aged two, twelve and 18 months for four weeks.

Afterwards, they tested learning capacity and memory performance in the animals -- orientation skills and the recognition of other mice. Mice who were only given a placebo displayed natural age-dependent learning had memory losses.

In contrast, the cognitive functions of the animals treated with cannabis were just as good as the two-month-old control animals. The treatment completely reversed the loss of performance in the old animals.

Scientists discovered that the brain ages much faster when mice do not possess any functional receptors for THC. These cannabinoid 1 (CB1) receptors are proteins to which the substances dock and thus trigger a signal chain. CB1 is also the reason for the intoxicating effect of THC in cannabis products, such as hashish or marijuana, which accumulate at the receptor.

THC imitates the effect of cannabinoids produced naturally in the body, which fulfil important functions in the brain. With increasing age, the quantity of the cannabinoids naturally formed in the brain reduces.

When the activity of the cannabinoid system declines, we find rapid ageing in the brain. To discover precisely what effect the THC treatment has in old mice, the researchers examined the brain tissue and gene activity of the treated mice.

The molecular signature no longer corresponded to that of old animals, but similar to that of young animals. The number of links between the nerve cells in the brain also increased again, which is an important for learning ability.

A low dose of the administered THC was chosen so that there was no intoxicating effect in the mice. Cannabis products are already permitted as medications, for instance as pain relief. As a next step, the researchers want to conduct a clinical trial to investigate whether THC also reverses ageing processes in human brain and can increase cognitive ability.

Links between blood sugar and brain cancer

Diabetes and elevated blood sugar increase the risk of different types of cancer.

Human brain accounts for 2 percent of body weight but consumes about 20 percent of body's glucose.

Brain tumors are common among people who have normal levels of blood glucose than those with high blood sugar or diabetes.

Glioma is one of the most common types of cancerous tumors originating in the brain. It begins in the cells that surround nerve cells.

This shows that elevated blood sugar may be associated with a protective factor that reduces brain tumor risk

Insulin-like growth factor is associated with glioma recurrence and is found in lower levels in people with diabetes than those who don't have the disease.

Umbilical cord protein may restore the aging brain

Researchers at Stanford University School of Medicine in California discovered umbilical cord blood to restore the learning ability that declines with age.

Injecting older mice with human umbilical cord blood revitalized mice's brain function, researchers suggest it may do the same in human brain.

Hippocampal part of the brain is responsible for converting experiences in to long-term memories can't function properly as we increase in age because it will loses nerve cells and shrinks.

Human and mice have tissue inhibitor of metalloproteases 2 (TIMP 2) in common, the protein improved nerve-cell activity in the brain in a laboratory experiment.

TIMP 2 was injected into older mice and it replicated the positive effects of the umbilical cord, scientists confirmed that umbilical cord plasma  improved hippocampal function in mice.