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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Amantadine for treating Parkinson's disease

FDA Approves Osmolex ER (amantadine) for the treatment of Parkinson’s disease and drug-Induced extrapyramidal reactions. Amantadine is an antiviral medicine that blocks the actions of viruses in the body. It is used to treat or prevent influenza A in adults and children. It may not be effective during every flu season because certain strains of the virus may be resistant to this medicine. It should not be used in place of getting a yearly flu shot.

Amantadine is also used to treat "Parkinson-like" symptoms such as stiffness or tremors, shaking, and repetitive uncontrolled muscle movements that may be caused by the use of certain drugs.

Amantadine side effects
Get emergency medical help if you have signs of an allergic reaction: hives ; difficult breathing; swelling of your face, lips, tongue, or throat. Call your doctor at once if you have: extreme drowsiness, falling asleep suddenly even after feeling alert; a light-headed feeling, like you might pass out; shortness of breath (even with mild exertion), swelling in your hands or feet;
painful or difficult urination; depression, agitation, aggression, behavior changes, hallucinations, thoughts of hurting yourself; a seizure; or severe nervous system reaction-very stiff (rigid) muscles, high fever, sweating, confusion, fast or uneven heartbeats and tremors.
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Calcium may cause Parkinson's disease

The international team, led by the University of Cambridge, found that calcium can mediate the interaction between small membranous structures inside nerve endings, which are important for neuronal signalling in the brain, and alpha-synuclein, the protein associated with Parkinson's disease. Excess levels of either calcium or alpha-synuclein may be what starts the chain reaction that leads to the death of brain cells.

Parkinson's disease is one of a number of neurodegenerative diseases caused when naturally occurring proteins fold into the wrong shape and stick together with other proteins, eventually forming thin filament-like structures called amyloid fibrils. These amyloid deposits of aggregated alpha-synuclein, also known as Lewy bodies, are the sign of Parkinson's disease.

Curiously, it hasn't been clear until now what alpha-synuclein actually does in the cell: why it's there and what it's meant to do. It is implicated in various processes, such as the smooth flow of chemical signals in the brain and the movement of molecules in and out of nerve endings, but exactly how it behaves is unclear.

"Alpha-synuclein is a very small protein with very little structure, and it needs to interact with other proteins or structures in order to become functional, which has made it difficult to study," said senior author Dr Gabriele Kaminski Schierle from Cambridge's Department of Chemical Engineering and Biotechnology.

Super-resolution microscopy techniques makes it possible to look inside cells to observe the behaviour of alpha-synuclein. To do so, researchers isolated synaptic vesicles, part of the nerve cells that store the neurotransmitters which send signals from one nerve cell to another.

In neurons, calcium plays a role in the release of neurotransmitters. The researchers observed that when calcium levels in the nerve cell increase, such as upon neuronal signalling, the alpha-synuclein binds to synaptic vesicles at multiple points causing the vesicles to come together. This may indicate that the normal role of alpha-synuclein is to help the chemical transmission of information across nerve cells.

There is a fine balance of calcium and alpha-synuclein in the cell, and when there is too much of one or the other, the balance is tipped and aggregation begins, leading to Parkinson's disease. The imbalance can be caused by a genetic doubling of the amount of alpha-synuclein (gene duplication), by an age-related slowing of the breakdown of excess protein, by an increased level of calcium in neurons that are sensitive to Parkinson's, or an associated lack of calcium buffering capacity in these neurons.

Understanding the role of alpha-synuclein in physiological or pathological processes may aid in the development of new treatments for Parkinson's disease. One possibility is that drug candidates developed to block calcium, for use in heart disease for instance, might also have potential against Parkinson's disease.
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Brain zaps for Tourette syndrome

Electric zaps can rewire the brains of Tourette syndrome patients, effectively reducing their uncontrollable vocal and motor tics. The procedure, called deep brain stimulation (DBS), improved tic severity by nearly half in patients with uncontrolled Tourette symptoms.

According to Dr. Michael Okun, chair of neurology and co-director of the Movement Disorders Center at the University of Florida's College of Medicine, much improvement in these symptoms is difficult when using medication or behavioral therapy.

With DBS, brain surgeons run thin electric leads to specific regions of the basal ganglia, a cluster of nerves in the brain related to motor control and behavior, then apply electricity to the brain circuits they've most closely linked to Tourette, to try to control the patient's tics. then introduce electricity into the brain to change the way these circuits function.

However, the procedure still needs more work. More than a third of patients experienced adverse events, most often slurred speech or a pins-and-needles sensation. These side effects occur when electricity meant for one brain circuit unintentionally spreads to other nearby nerves but the adverse effects are reversible.

Tourette patients are typically treated using medications and speech or behavioral therapy. Another option for severe Tourette cases is deep brain stimulation, which also used to treat many other motor disorders, including Parkinson's disease, essential tremor and multiple sclerosis.

Researchers wanted a better idea of whether DBS is effective in treating severe cases of uncontrolled Tourette, which can cause motor tics so strong that people end up hurting themselves. The average tic severity patients that used DBS improved by 45 percent within one year of implant.
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Brain cells may prevent Parkinson's disease

A Norwegian study shows that impairment in mitochondria may actually protect the brain in Parkinson's disease. Mitochondria are microscopic power stations found inside human cells. They convert foodstuffs into fuel, providing the required energy. Studies in brain tissue from individuals with Parkinson's disease showed that an essential component of the mitochondrial energy generators, called respiratory complex-I, becomes impaired in an area of the brain called the "substantia nigra" .

A new study from the University of Bergen (UiB), in Norway, in collaboration with the University of Cambridge, shows that the function of mitochondria, the microscopic powerhouses of the cell, is altered throughout the entire brain of individuals with Parkinson's disease. This new study shows that complex I deficiency is a global phenomenon in the brain of people with Parkinson's disease, and is found indiscriminately in both affected and healthy brain regions.

 Intriguingly, brain cells (neurons) with decreased complex I levels are significantly less likely to contain Lewy bodies, the abnormal protein-aggregates that characterize Parkinson's disease. These discoveries suggest that, contrary to mainstream theory, mitochondrial complex I deficiency may not be entirely deleterious for the brain in Parkinson's disease. It is possible that complex I deficiency is part of a compensatory regulation attempting to protect the brain in Parkinson's disease.

Parkinson's disease is one of the most common brain disorders. It affects millions of people worldwide. It starts after the age of 50 and causes a combination of debilitating symptoms, including shaking and other abnormal movements, loss of balance, low blood pressure, bladder and intestinal problems, sleeping disorders and dementia. Presently, there is no cure and patients die prematurely due to increasing disability.
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Links between Crohn's and Parkinson's disease

Mount Sinai Researchers have just discovered that patients in the Ashkenazi Jewish population with Crohn's disease (a chronic inflammatory of the digestive system) are more likely to carry the LRRK2 gene mutation. This gene is the major genetic cause of Parkinson's disease, which is a movement disorder.

Crohn's disease is a complex disorder with multiple genes and environmental factors involved, which disproportionally affects individuals of Ashkenazi Jewish ancestry. The presence of shared LRRK2 mutations in patients with Crohn's disease and Parkinson's disease provides refined insight into disease mechanisms and may have major implications for the treatment of these two seemingly unrelated diseases.

Researchers used international data from the last decade up to the present to analyze the occurrence of some coding genetic mutations in the human genome of many  patients with Crohn's disease and compared them to people without the disorder. They identified mutations in the LRRK2 gene that are more frequently found in Crohn's disease cases as compared to unaffected individuals.

When they discovered a link between Crohn's and the LRRK2 gene mutations they went further to assess the possible genetic link between Crohn's and Parkinson's. The team then looked at a much larger sample of people including patients with Crohn's, Parkinson's, and no disease.

The study found two mutations of the LRRK2 gene in Crohn's disease patients. One of them called the risk mutation was more common in patients with Crohn's, while the other (the protective mutation) was more prevalent in patients without the disease. Most Crohn's disease patients who carried the risk mutation developed the disease on average six years earlier than those who did not carry this mutation.

The research also shows that more Crohn's patients with the risk mutation developed the disease in the small intestine, compared to those without the mutation. If the disease starts in the small intestine, it becomes more difficult to manage and often leads to complications and surgeries.
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Dangers of using anaesthetics

A new understanding of the complex ways in which general anaesthetics act on the brain could eventually lead to improved drugs for surgery. It remains unclear how general anaesthesia works, even though it is one of the most common medical procedures worldwide.

University of Queensland researcher, Associate Professor Bruno van Swinderen, said his team had overturned previous understanding of what general anaesthetics do to the brain, finding the drugs did much more than induce sleep.

Researchers looked at the effects of propofol - one of the most common general anaesthetic drugs used during surgery - on synaptic release. Synaptic release is the mechanism by which neurons - or  nerve cells - communicate with each other.

From the previous research that general anaesthetics including propofol act on sleep systems in the brain like a sleeping pill. This study discovered that propofol also disrupts presynaptic mechanisms, probably affecting communication between neurons across the entire brain in a systematic way that differs from just being asleep.

 Propofol restricts the movement of a key protein (syntaxin1A) required at the synapses of all neurons. This restriction leads to decreased communication between neurons in the brain. The finding contributed to understanding how general anaesthetics worked, and could explain why people experienced grogginess and disorientation after coming out of surgery.

The discovery has implications for people whose brain connectivity is vulnerable, for example in children whose brains are still developing or for people with Alzheimer's or Parkinson's disease.
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Autoimmunity contributes to Parkinson's disease

 Autoimmunity  is when the immune system attacks the body's own tissues. Parkinson's disease is neurodegenerative movement disorder.
Malfunctioning immune system contributes to Parkinson's disease.

Two fragments of alpha-synuclein, a protein that accumulates in the brain cells of Parkinson's disease patients can activate the T cells involved in autoimmune attacks.

Dopamine neurons that are affected by Parkinson's disease are vulnerable because they have proteins on the cell surface that help the immune system recognize foreign substances.

 Researchers examined blood samples from 67 Parkinson's disease patients and 36 healthy controls to fragments of alpha-synuclein and other proteins found in neurons.

 The immune response was associated with a common form of a gene found in the immune system, which may explain why many people with Parkinson's disease carry this gene variant.

 Immunotherapy can be used to increase the immune system's tolerance for alpha-synuclein, which could help to prevent worst condition of Parkinson's disease.

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Dairy products increase the risk of Parkinson's disease

Consuming three servings of low-fat dairy a day is associated with the risk of developing Parkinson's disease.

Drinking more than one serving of low-fat or skim milk per day is associated with a greater risk of developing Parkinson's disease.

Researchers analyzed approximately 25 years of data on 80,736 women enrolled in the Nurses' Health Study and 48,610 men enrolled in the Health Professionals' Follow-up Study.

Participants in these studies completed health questionnaires every two years and diet questionnaires every four years. During that time, 1,036 people developed Parkinson's disease.

Researchers examined what kinds of dairy each person consumed, including milk, cream, cheese, yogurt, ice cream, butter, margarine and sherbet.

 Full-fat dairy, like whole milk is not associated with the risk of Parkinson's disease. Regular intake of dairy products is associated with increased risk of Parkinson's disease.


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How Parkinson's disease start

Parkinson's disease is a progressive disorder of the nervous system that affects movement.

Bojing Liu of the Karolinska Instituet in Stockholm, Sweden and colleagues discovered that Parkinson's disease might start in the gut and move to the brain through the vagus nerve.

The vagus nerve is the longest cranial nerve, it has motor and sensory fibres because it passes through the neck to the abdomen.

Researchers analyzed registers in Sweden to compare 9,430 people who had a vagotomy over a 40 years to 377,200 people from the general population.

At that time, 101 people who had a vagotomy developed Parkinson's disease. After adjusting for condition
like chronic obstructive pulmonary disease, diabetes, vascular disease, rheumatologic disease and osteoarthritis.

People who had a truncal vagotomy five years earlier may not develop Parkinson's disease compare to those who had not had the surgery.

Those who will develop Parkinson's disease in future have a protein responsible for the disease in there gut.