alzheimer’s

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Why nutritional psychiatry is the future of mental health treatment

Blueberries

Very interesting and may be so helpful.

Below is a direct quote from the article below. I wonder why we are not told to add vitamin and mineral as well as OTC anti-inflammatory supplementation to out diets and medicine regimen? It would be worth it to try it, if it doesn’t help, ok, but imagine it does help! I am going to ask my psychiatrist about all of these and if they have any adverse reactions with the medications I’m on. That’s would be the best way to go here. Wishing us all the best of physical and mental health.

“It is now known that many mental health conditions are caused by inflammation in the brain which ultimately causes our brain cells to die. This inflammatory response starts in our gut and is associated with a lack of nutrients from our food such as magnesium, omega-3 fatty acids, probiotics, vitamins and minerals that are all essential for the optimum functioning of our bodies. Recent research has shown that food supplements such as zinc, magnesium, omega 3, and vitamins B and D3 can help improve people’s mood, relieve anxiety and depression and improve the mental capacity of people with Alzheimer’s. Magnesium is one of most important minerals for optimal health, yet many people are lacking in it. One study found that a daily magnesium citrate supplement led to a significant improvement in depression and anxiety, regardless of age, gender or severity of depression. Improvement did not continue when the supplement was stopped. Omega-3 fatty acids are another nutrient that is critical for the development and function of the central nervous system – and a lack has been associated with low mood, cognitive decline and poor comprehension. Research has shown that supplements like zinc, magnesium and vitamins B and D can improve the mental capacity of people with Alzheimer’s. Shutterstock The role of probiotics – the beneficial live bacteria in your digestive system – in improving mental health has also been explored by psychiatrists and nutritionists, who found that taking them daily was associated with a significant reduction in depression and anxiety. Vitamin B complex and zinc are other supplements found to reduce the symptoms of anxiety and depression. Hope for the future? These over-the-counter” supplements are widely available in supermarkets, chemists and online health food stores, although the cost and quality may vary. For people who have not responded to prescription drugs or who cannot tolerate the side effects, nutritional intervention can offer hope for the future. There is currently much debate over the effectiveness of antidepressants. The use of food supplements offer an alternative approach that has the potential to make a significant difference to the mental health of all age groups.”

 

http://theconversation.com/why-nutritional-psychiatry-is-the-future-of-mental-health-treatment-92545

A lack of essential nutrients is known to contribute to the onset of poor mental health in people suffering from anxiety and depression, bipolar disorder, schizophrenia and ADHD. Nutritional psychiatry is a growing discipline that focuses on the use of food and supplements to provide these essential nutrients as part of an integrated or alternative treatment for mental health disorders. But nutritional approaches for these debilitating conditions are not widely accepted by mainstream medicine. Treatment options tend to be limited to official National Institute for Care Excellence (NICE) guidelines which recommend talking therapies and antidepressants. Use of antidepressants Antidepressant use has more than doubled in recent years. In England 64.7m prescriptions were issued for antidepressants in 2016 at a cost of £266.6m. This is an increase of 3.7m on the number of items prescribed in 2015 and more than double than the 31m issued in 2006. A recent Oxford University study found that antidepressants were more effective in treating depression than placebo. The study was led by Dr Andrea Cipriani who claimed that depression is under treated. Cipriani maintains that antidepressants are effective and a further 1m prescriptions should be issued to people in the UK. This approach suggests that poor mental health caused by social conditions is viewed as easily treated by simply dispensing drugs. But antidepressants are shunned by people whom they could help because of the social stigma associated with mental ill-health which leads to discrimination and exclusion. Prescriptions for 64.7m items of antidepressants were dispensed in England in 2016, the highest level recorded by the NHS. Shutterstock More worrying is the increase in the use of antidepressants by children and young people. In Scotland, 5,572 children under 18 were prescribed antidepressants for anxiety and depression in 2016. This figure has more than doubled since 2009/2010. But according to British psychopharmacologist Professor David Healy, 29 clinical trials of antidepressant use in young people found no benefits at all. These trials revealed that instead of relieving symptoms of anxiety and depression, antidepressants caused children and young people to feel suicidal. Healy also challenges their safety and effectiveness in adults. He believes that antidepressants are over-prescribed and that there is little evidence that they are safe for long-term use. Antidepressants are said to create dependency, have unpleasant side effects and cannot be relied upon to always relieve symptoms. Nutrition and poor mental health In developed countries such as the UK we eat a greater variety of foodstuffs than ever before – but it doesn’t follow that we are well nourished. In fact, many people do not eat enough nutrients that are essential for good brain health, opting for a diet of heavily processed food containing artificial additives and sugar. The link between poor mental health and nutritional deficiencies has long been recognised by nutritionists working in the complementary health sector. However, psychiatrists are only now becoming increasingly aware of the benefits of using nutritional approaches to mental health, calling for their peers to support and research this new field of treatment. It is now known that many mental health conditions are caused by inflammation in the brain which ultimately causes our brain cells to die. This inflammatory response starts in our gut and is associated with a lack of nutrients from our food such as magnesium, omega-3 fatty acids, probiotics, vitamins and minerals that are all essential for the optimum functioning of our bodies. Recent research has shown that food supplements such as zinc, magnesium, omega 3, and vitamins B and D3 can help improve people’s mood, relieve anxiety and depression and improve the mental capacity of people with Alzheimer’s. Magnesium is one of most important minerals for optimal health, yet many people are lacking in it. One study found that a daily magnesium citrate supplement led to a significant improvement in depression and anxiety, regardless of age, gender or severity of depression. Improvement did not continue when the supplement was stopped. Omega-3 fatty acids are another nutrient that is critical for the development and function of the central nervous system – and a lack has been associated with low mood, cognitive decline and poor comprehension. Research has shown that supplements like zinc, magnesium and vitamins B and D can improve the mental capacity of people with Alzheimer’s. Shutterstock The role of probiotics – the beneficial live bacteria in your digestive system – in improving mental health has also been explored by psychiatrists and nutritionists, who found that taking them daily was associated with a significant reduction in depression and anxiety. Vitamin B complex and zinc are other supplements found to reduce the symptoms of anxiety and depression. Hope for the future? These over-the-counter” supplements are widely available in supermarkets, chemists and online health food stores, although the cost and quality may vary. For people who have not responded to prescription drugs or who cannot tolerate the side effects, nutritional intervention can offer hope for the future. There is currently much debate over the effectiveness of antidepressants. The use of food supplements offer an alternative approach that has the potential to make a significant difference to the mental health of all age groups. The emerging scientific evidence suggests that there should be a bigger role for nutritional psychiatry in mental health within conventional health services. If the burden of mental ill health is to be reduced, GPs and psychiatrists need to be aware of the connection between food, inflammation and mental illness. Medical education has traditionally excluded nutritional knowledge and its association with disease. This has led to a situation where very few doctors in the UK have a proper understanding of the importance of nutrition. Nutritional interventions are thought to have little evidence to support their use to prevent or maintain well-being and so are left to dietitians, rather than doctors, to advise on. But as the evidence mounts up, it is time for medical education to take nutrition seriously so that GPs and psychiatrists of the future know as much about its role in good health as they do about anatomy and physiology. The state of our mental health could depend on it.

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It’s the Immune System!

DSCN5325

In normal brains, the number of synapses (connections between neurons where neurotransmitters act and brain activity takes place and nerve impulses and information is passes on) is pruned or  whittled down as the brain matures from the womb to adolescence. These synapses are eliminated by immune cells of the brain called microglia.

First the hypothesis that Schizophrenia is caused by activation of microglia which eat away at synapses in childhood or adolescence, leading to fewer synapses and this mental illness! An amazing paper about which I wrote a post (https://wordpress.com/post/bipolar1blog.wordpress.com/3623) C1q is a protein that tags the neuronal synapses, once a synapse is tagged, microglia (the immune cells of the brain) come and chomp it away, voila, no more synapse. The information that that one synapse was transmitting is now lost. If this happens to many, many, synapses, a lot of communication and information is lost. And this loss leads to schizophrenia!

Now the same observations about Alzheimer’s as well! Microglia are eating away too may synapses in areas of the brain that are key to memory. β Amyloid is a plaque of protein found to a much larger extent in the brains of people with Alzheimer’s. It is a deposit that is seen along neurons of people with Alzheimer’s. What this research team has found is that C1q in conjunction with the existence of β Amyloid plaques is what causes the microglia to eat up healthy synapses. This lead to destruction of brain cell connectivity, especially in the areas that house memory. So this process that happens naturally in the womb, somehow gets turned on later in life and causes pruning of connections in neurons which we need and leads to Alzheimer’s.

Again, it’s the immune system stupid!

http://www.sciencemag.org/news/2016/03/over-pruning-synapses-may-drive-early-stage-alzheimer-s-disease?utm_source=newsfromscience&utm_medium=facebook-text&utm_campaign=alzhapses-3346

Alzheimer’s may be caused by haywire immune system eating brain connections

More than 99% of clinical trials for Alzheimer’s drugs have failed, leading many to wonder whether pharmaceutical companies have gone after the wrong targets. Now, research in mice points to a potential new target: a developmental process gone awry, which causes some immune cells to feast on the connections between neurons.

“It is beautiful new work,” which “brings into light what’s happening in the early stage of the disease,” says Jonathan Kipnis, a neuroscientist at the University of Virginia School of Medicine in Charlottesville.

Most new Alzheimer’s drugs aim to eliminate β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. Those with Alzheimer’s tend to have more of these deposits in their brains than do healthy people, yet more plaques don’t always mean more severe symptoms such as memory loss or poor attention, says Beth Stevens of Boston Children’s Hospital, who led the new work.

What does track well with the cognitive decline seen in Alzheimer’s disease—at least in mice that carry genes that confer high risk for the condition in people—is a marked loss of synapses, particularly in brain regions key to memory, Stevens says. These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity.

Stevens has spent much of her career studying a normal immune mechanism that prunes weak or unnecessary synapses as the brain matures from the womb through adolescence, allowing more important connections to become stronger. In this process, a protein called C1q sets off a series of chemical reactions that ultimately mark a synapse for destruction. After a synapse has been “tagged,” immune cells called microglia—the brain’s trash disposal service—know to “eat” it, Stevens says. When this system goes awry during the brain’s development, whether in the womb or later during childhood and into the teen years, it may lead to psychiatric disorders such as schizophrenia, she says.

Stevens hypothesized that the same mechanism goes awry in early Alzheimer’s disease, leading to the destruction of good synapses and ultimately to cognitive impairment. Using two Alzheimer’s mouse models—each of which produces excess amounts of the β amyloid protein, and develops memory and learning impairments as they age—she and her team found that both strains had elevated levels of C1q in brain tissue. When they used an antibody to block C1q from setting off the microglial feast, however, synapse loss did not occur, the team reports today in Science.

To Stevens, that suggests that the normal mechanism for pruning synapses during development somehow gets turned back on again in the adult brain in Alzheimer’s, with dangerous consequences. “Instead of nicely whittling away [at synapses], microglia are eating when they’re not supposed to,” she says.

The group is now tracking these mice to see whether a drug that blocks C1q slows their cognitive decline. To determine whether elevated β amyloid can cause the C1q system to go haywire, Stevens and colleagues also injected a form of the protein which is known to generate plaques into the brains of normal mice and so-called knockouts that could not produce C1q because of a genetic mutation. Although normal mice exposed to the protein lost many synapses, knockouts were largely unaffected, Stevens says. In addition, microglia only went after synapses when β amyloid was present, suggesting that the combination of protein and C1q is what destroys synapses, rather than either element alone, she says, adding that other triggers, such as inflammatory molecules called cytokines, might also set the system off.

The findings contradict earlier theories which held that increased microglia and C1q activity were merely part of an inflammatory reaction to β amyloid plaques. Instead, microglia seem to start gorging on synapses long before plaques form, Stevens says. She and several co-authors are shareholders in Annexon Biosciences, a biotechnology company that will soon start testing the safety of a human form of the antibody the team used to block C1q, known as ANX-005, in people.

Such a central role for microglia in Alzheimer’s disease is “still on the controversial side,” says Edward Ruthazer, a neuroscientist at the Montreal Neurological Institute and Hospital in Canada. One “really compelling” sign that the mechanism is important in people would be if high levels of C1q in cerebrospinal fluid early on predicted developing full-blown Alzheimer’s later in life, he says. Still, he says, “it’s difficult to argue with the strength of the study’s evidence.”

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Blocking inflammation prevents cell death, improves memory in Alzheimer’s disease

 Once again, the immune system, specifically inflammation, plays a huge role in Alzheimer’s, a neurodegenerative disease. Mental illness, in some ways, is very close to a neurodegenerative disease. I wonder, I always wonder, what if it’s the immune system and inflammation that is responsible for diseases such as bipolar d/o or schizophrenia. 

http://www.neuroscientistnews.com/research-news/blocking-inflammation-prevents-cell-death-improves-memory-alzheimers-disease

Using a drug compound created to treat cancer, University of California, Irvine (UCI) neurobiologists have disarmed the brain’s response to the distinctive beta-amyloid plaques that are the hallmark of Alzheimer’s disease.
Kim Green and colleagues with UCI’s Institute for Memory Impairments and Neurological Disorders found that flushing away the abundant inflammatory cells produced in reaction to beta-amyloid plaques restored memory function in test mice. Their study showed that these microglia cells contribute to the neuronal and memory deficits seen in this neurodegenerative disease. Results appear in the journal Brain.

“Our findings demonstrate the critical role that inflammation plays in Alzheimer’s-related memory and cognitive losses,” said Green, an assistant professor of neurobiology & behavior. “While we were successful in removing the elevated microglia resulting from beta-amyloid, further research is required to better understand the link among beta-amyloid, inflammation and neurodegeneration in Alzheimer’s.”  

The neurobiologists treated Alzheimer’s disease model mice with a small-molecule inhibitor compound called pexidartinib, or PLX3397, which is currently being used in several phase 2 oncology studies and a phase 3 clinical trial to treat a benign neoplasm of the joints.
The inhibitor works by selectively blocking signaling of microglial surface receptors, known as colony-stimulating factor 1 receptors, which are necessary for microglial survival and proliferation in response to various stimuli, including beta-amyloid. This led to a dramatic reduction of these inflammatory cells, allowing for analysis of their role in Alzheimer’s. The researchers noted a lack of neuron death and improved memory and cognition in the pexidartinib-treated mice, along with renewed growth of dendritic spines that enable brain neurons to communicate.
Green said that although the compound swept away microglia, the beta-amyloid remained, raising new questions about the part these plaques play in Alzheimer’s neurodegenerative process.
In healthy tissue, microglia act as the first and main form of immune defense in the central nervous system. But in a disease state, such as Alzheimer’s, microglia appear to turn against the healthy tissue they were originally assigned to protect, causing inflammation in the brain. The beta-amyloid plaques in brain areas related to Alzheimer’s disease are rich with these rogue microglia, Green added.
“Our work is telling us that these cells may contribute to the disease process, and targeting them with such specific drugs is a promising new approach,” he said.

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New data shows monoclonal antibodies may indeed slow the disease when given early

http://www.scientificamerican.com/article/pharma-watch-the-promise-of-alzheimer-s-drugs-revived/
With millions of baby boomers fast approaching old age, Alzheimer’s disease diagnoses are set to spike—and the hunt is on to find medications that can slow or halt the progression of this most common form of dementia. Many pharmaceutical companies pinned high hopes on monoclonal antibodies, drugs designed to latch onto a toxic protein that builds up in the brain of sufferers and triggers the immune system to break it down. In preliminary studies during the past decade, however, these drugs often failed to outperform placebos. Now several new analyses may have resurrected their original promise.

In July three research teams presented data at the Alzheimer’s Association International Conference in Washington, D.C., suggesting that monoclonal antibodies could potentially stall Alzheimer’s relentless progression—provided they could be given early enough and at high-enough doses. These experimental drugs all target beta-amyloid, a protein fragment at the heart of a widely accepted theory about how Alzheimer’s destroys memory. Every cell in the body produces beta-amyloid, but if the brain cannot clear it fast enough, it starts to clump together, gumming up synapses and amassing into neuron-killing plaques. Antiamyloid monoclonal antibodies are designed to bind to the fragments and flag them for removal by the immune system.

At the meeting, pharmaceutical company Biogen presented new findings from an ongoing study of its monoclonal candidate, aducanumab. Biogen had announced with much fanfare in March that the drug significantly reduced beta-amyloid plaques seen on PET scans and slowed cognitive impairment in 166 patients with mild Alzheimer’s. Patients on the top dose tested—10 milligrams per kilogram of body weight—maintained the highest memory scores but also experienced more localized brain swelling, a side effect linked to leaky blood vessels. So midtrial they introduced what they hoped would be a Goldilocks dose—not too much, not too little. But it was not just right. Biogen’s researchers revealed that six milligrams produced even less benefit than three milligrams on one measure of cognitive function. The search for the perfect dose, and definitive proof of the drug’s potency, will continue during an upcoming five-year study.

In the meantime, researchers at Eli Lilly described potentially encouraging results from an extension of a large failed trial of solanezumab. To highlight this monoclonal antibody’s efficacy, they focused only on patients with early disease and used a so-called delayed-start analysis—the first ever for an Alzheimer’s drug. At the start of the 3.5-year trial, they randomly assigned 1,322 patients to either placebo or active treatment. After 80 weeks, everyone in the placebo group began taking solanezumab as well.

Both groups continued to show worsening symptoms, but treatment seemed to slow the pace by about one third. Of significance, the placebo group never caught up to the cognitive scores of patients who received solanezumab from the start. The researchers interpret this finding as tantalizing evidence that the drug is mopping up beta-amyloid in the brain and tempering its toxicity. If it were simply treating symptoms, the delayed-start control group should have made the same gains as the first group—just later on. A confirmation study is under way.

And scientists at Hoffmann–La Roche have described new findings about yet another antiamyloid drug, gantenerumab. A large trial of this monoclonal antibody was canceled in December 2014, when it failed to show any measurable effects. Yet when the researchers reanalyzed the data, considering only patients with very early and rapidly progressing disease, they found that gantenerumab had reduced beta-amyloid on PET scans for that group. It also reduced levels of tau—another protein that builds up inside neurons as Alzheimer’s advances, forming tangles that fritz normal cell function.

All three reports underscore the importance of early intervention. At a certain point, it may be too late to stem the amyloid tide. Several other trials are now probing whether antiamyloid drugs might be even more powerful when used preventively. The so-called A4 study, a joint effort of the National Institutes of Health, Eli Lilly and several nonprofit organizations, is testing solanezumab in patients who do not yet display memory deficits but have increased levels of beta-amyloid on PET scans. Two more investigations are exploring solanezumab’s effect on healthy people who carry genetic mutations that put them at high risk for inheriting Alzheimer’s.

For all the rekindled hope around monoclonal antibodies, other classes of drugs in earlier stages of testing may wind up doing as much or more to help Alzheimer’s patients. “Some of the most advanced stages of development are in drugs targeting beta-amyloid,” says Heather Snyder, director of medical and scientific operations at the Alzheimer’s Association, “but there are other clinical trials targeting insulin, tau, inflammation, and mechanisms behind neuron growth and health. We will need to identify all the biological changes taking place and intervene with all the treatments we have available—both medications and lifestyle changes—if we are going to reduce the risk or stop or slow the progression of Alzheimer’s.”

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DNA Repair Protein BRCA1 Implicated in Cognitive Function and Dementia

BRCA1 in neurons_2130x1198

Wow! The BRCA1 gene, mutations in which lead to breast cancer, has now been implicated in cognitive functioning, dementia and the development of Alzheimer’s disease!

BRCA1 is a tumor suppressor gene, this encodes a protein that repairs DNA mutations. If these mutations in the DNA were not repaired, the cell would become cancerous. So the repair of these mutations suppresses tumor formation, hence the term tumor suppressor gene. If there is a mutation in BRCA1, the mutations in DNA will not be properly repaired and can lead to oncogenesis.

What’s very surprising is that these genes, first discovered in relation to breast cancer, have now been seen to have an important role in neurons! In post mortem studies, it was seen that BRCA1 was 65-75% lower in patients who had dementia than in normal controls. It was found that β amyloid (the proteins that accumulate in brains of people with Alzheimer’s,) depletes BRCA1 in neurons. Faulty DNA repair was known to occur in the neurons of people with Alzheimer’s, now with the involvement of BRCA1, it makes perfect sense.

BRCA1 is involved in Alzheimer’s disease, wow! Could it or some other DNA repair proteins be involved in mental illness?

As I said in another post about why elephants don’t get cancer (https://bipolar1blog.wordpress.com/2015/10/11/wow-this-is-the-reason-why-elephants-dont-get-cancer/), elephants have 40 copies of a particular tumor suppressor gene called p53, whereas humans have two. I wonder if overproducing BRCA1 in neurons, either by increasing the number of its gene or by delivering the BRCA1 protein in nanoparticles into the neurons of people with dementia, would that halt dementia, or at least slow it down?

Curiouser and curiouser… it is all interconnected!

Breast cancer proteins seen in dementia; neurotransmitters, neuronal messengers, seen in the gut and muscles; interleukins, immune cell molecules, present in the brain…

http://gladstone.org/about-us/news/dna-repair-protein-brca1-implicated-cognitive-function-and-dementia