Behavior, brain SPECT scan, hormones, gratitude, neuroplasticity

Neuroplasticity, also known as brain plasticity, is an umbrella term that describes lasting change to the brain throughout an individual’s life course. The term gained prominence in the latter half of the 20th century, when new research[1] showed many aspects of the brain remain changeable (or “plastic”) even into adulthood.[2] This notion contrasts with the previous scientific consensus that the brain develops during a critical period in early childhood, then remains relatively unchangeable (or “static”) afterward.[3]

Neuroplastic change can occur at small scales, such as physical changes to individual neurons, or at whole-brain scales, such as cortical remapping in response to injury; however cortical remapping only occurs during a certain time period meaning that if a child were injured and it resulted in brain damage then cortical remapping would most likely occur, however if an adult was injured and it resulted in brain damage, then cortical remapping would not occur since the brain has made the majority of its connections.[4] Behavior, environmental stimuli, thought, and emotions may also cause neuroplastic change through activity-dependent plasticity, which has significant implications for healthy development, learning, memory, and recovery from brain damage.[4][5][6]

Neuroscientists distinguish synaptic plasticity, which refers to changes in how neurons connect to each other, from non-synaptic plasticity, which refers to changes in the neurons themselves.

Chronic pain

Main article: Chronic pain

Individuals who suffer from chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from periphery then elicit a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.[32] For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth.[33] Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus.[34] However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain,[35] chronic low back pain[36] and carpal tunnel syndrome.[37]

Meditation

A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter.[38][39][40] One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000.[41] Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest that long-term, or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as attention, anxiety, depression, fear, anger, the ability of the body to heal itself, and so on. These functional changes may be caused by changes in the physical structure of the brain.[42][43][44][45]

Fitness and exercise

Aerobic exercise promotes adult neurogenesis by increasing the production of neurotrophic factors (compounds that promote growth or survival of neurons), such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 (IGF-1), and vascular endothelial growth factor (VEGF).[46][47][48] Exercise-induced neurogenesis in the hippocampus is associated with measurable improvements in spatial memory.[49][50][51][52] Consistent aerobic exercise over a period of several months induces marked clinically significant improvements in executive function (i.e., the “cognitive control” of behavior) and increased gray matter volume in multiple brain regions, particularly those that give rise to cognitive control.[48][49][53][54] The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex and hippocampus;[48][49][50] moderate improvements seen in the anterior cingulate cortex, parietal cortex, cerebellum, caudate nucleus, and nucleus accumbens.[48][49][50] Higher physical fitness scores (measured by VO2 max) are associated with better executive function, faster processing speed, and greater volume of the hippocampus, caudate nucleus, and nucleus accumbens.[49]

Human echolocation

Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010[55] and 2011[56] using functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation. Studies with blind patients, for example, suggest that the click-echoes heard by these patients were processed by brain regions devoted to vision rather than audition.[57]

ADHD stimulants

Reviews of magnetic resonance imaging (MRI) studies on individuals with ADHD suggest that the long-term treatment of attention deficit hyperactivity disorder (ADHD) with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudate nucleus of the basal ganglia.[58][59][60] Based upon rodent models, the authors of one review proposed that “juvenile exposure to methylphenidate may cause abnormal prefrontal function and impaired plasticity in the healthy brain”.[61] The same authors noted in another review that in juvenile rats, methylphenidate reduced levels of NR2B subunit of the NMDA receptor without altering NR2A levels in the prefrontal cortex, thereby affecting long-term plasticity in the prefrontal cortex.[

brain  101

Cancer diet, ketogenic – high fat

keto diet no carbs and supplements brain cancer

How a young man delayed cancer progression with high fat and less carbs diet, ketogenic diet?

He eats and fasts. He credits his health to whole foods of greens and dietary supplements. Fats are from coconut oil, omega 3, eggs, fish oil and other veggie sources.

Sugar is food for cancer cells. He avoid sugar and carbs rich in sugar and derives his carbs from greens.

Virus attacks cancer cells, healing brain tumors, a research from Duke University scientist

Modified poliovirus used as therapy for glioblastoma

The May 5, 2014 issue of People magazine features Stephanie Lipscomb, the first patient in the world to undergo an investigational therapy at Duke’s Preston Robert Tisch Brain Tumor Center, during which a modified poliovirus was injected into her brain to combat aggressive brain cancer. Two years after undergoing the procedure, Stephanie is doing great.

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DURHAM, N.C. — In a daring yet successful experiment to cure deadly brain tumors, researchers have combined the cancer-killing properties of poliovirus together with a harmless genetic coding element from the common cold. 

The resulting modified virus created a remarkably strong anti-cancer agent that rapidly killed cancer cells in laboratory cell cultures and in animals — and without causing polio, said Matthias Gromeier, M.D., assistant professor of molecular genetics and microbiology at the Duke Comprehensive Cancer Center. Testing of the new viral agent in humans should begin within two years, he said. 

In the study, the modified poliovirus rapidly killed cancer cells derived from primary brain tumors as well as cells derived from breast and colon cancer metastases — all within a matter of four to six hours. In fact, polio is known to be one of the quickest killers of infected host cells, producing approximately a thousand additional infectious viral units per infected cell, he said. 

“We made a drug out of a virus by engineering its destructive abilities from a foe into a friend,” said Gromeier. His most recent results — a collaborative effort with Darrell Bigner, M.D., Henry Friedman, M.D., Allan Friedman, M.D., and John Sampson, M.D., of the Brain Tumor Center at Duke — will be published in the Dec. 9, 2003, issue of the Proceedings of the National Academy of Sciences, which is currently available online. 

The key to Gromeier’s success has been disabling the poliovirus’ ability to kill normal brain cells while retaining its ability to kill cancer cells in the brain. To do so, Gromeier’s team swapped a critical genetic element from the common cold “rhinovirus” with the corresponding genetic element from the poliovirus. The genetic element, called an “IRES” (internal ribosomal entry site), enables a virus to express its own genetic information inside the host cell it has invaded, said Gromeier. 

Gromeier selected the IRES from a rhinovirus because it does not typically infect the human brain. Normal brain cells lack the appropriate environment required for the rhinovirus IRES to begin translating the poliovirus’s genetic information, his study demonstrated. 

Cancer cells, however, regulate gene expression very differently than normal cells do. They grow faster, lack growth inhibitors and generally provide a supportive environment that is highly susceptible to viruses of all sorts, making viruses an excellent invader to disrupt cancer’s growth. 

“In cancer cells, the IRES from rhinovirus acts as the trigger that activates gene expression, but the genes being expressed — the silver bullets in the gun, so to speak — are all from the poliovirus,” said Gromeier. “The polio proteins kill the cancer cells quickly and efficiently.” 

In fact, polio is the perfect virus to attack brain cancer cells because it has a natural affinity for invading the brain, said Gromeier. Polio infects brain cells by binding to a receptor or “docking site” called CD155 on the outside of motor neurons. Gromeier showed that brain tumors over-produce this CD155 receptor, making the cancer cells particularly vulnerable to infection with poliovirus. The modified poliovirus still enters normal motor neurons because it shares the same CD155 receptor as brain tumor cells, but it can no longer grow in normal cells. 

“We have a virus that naturally targets brain cells, but we have replaced the genetic coding element that makes the virus so dangerous,” said Gromeier. “The virus has lost its ability to grow in normal neurons.” 

Tests in mice and in non-human primates have confirmed that the modified poliovirus does, indeed, kill brain tumor cells but does not affect normal motor neurons. Moreover, viruses don’t carry the toxic side effects of chemotherapy and radiation, and viruses can be introduced directly into the tumor. 

“The brain is a very common site of cancer metastasis, but cancer in the brain is extremely difficult to treat,” said Gromeier. “Cancer cells are often interspersed throughout normal brain tissue, and most chemotherapy does not cross the blood-brain barrier, so getting the drug to the target site of treatment is a huge problem clinically.” 

To combat that problem, the modified poliovirus is directly injected into the brain tumor. Once there, the virus seeks out and destroys cancerous cells without detection by the body’s immune system. The immune system would normally neutralize the poliovirus in vaccinated individuals because they have built up antibodies against polio. But the brain does not have immunity against polio because antibodies do not cross the blood-brain barrier. Hence, infusing the brain directly with modified polio is the most effective method of killing cancer cells. 

But giving the modified poliovirus to humans — even to terminal brain cancer patients — requires rigorous testing to understand the mechanism behind its virulence in cancer cells and its impotence in normal brain cells. 

So, Gromeier’s team embarked on a mission to elucidate the molecular mechanism that causes the rhinovirus IRES to function in cancer cells but to malfunction in normal neurons. 

After extensive testing, he discovered that the IRES from the rhinovirus communicates with the opposite end of the poliovirus genome. That distant region, called the 3-prime non-translated region, drives how the virus transmits its genetic instructions inside the host cell. Gromeier’s data suggest that — in cancer cells — the rhinovirus IRES and the 3-prime communicate via a set of proteins, called co-factors, which ignite the IRES to begin functioning. 

Normal motor neurons, however, may not provide the appropriate set of co-factors to stimulate rhinovirus IRES function, said Gromeier. Hence, the modified virus cannot grow in normal motor neurons. 

“Cells differ in terms of how well-suited they are to a particular virus,” said Gromeier. “Every cell type has unique cellular proteins that can either support or block viral function, and we believe differences in these proteins account for the modified virus’ inability to infect normal brain cells.” 

The research was funded by the National Institutes of Health, the National Cancer Institute, The Burroughs Wellcome Fund, ABC2 Foundation, and the Brain Tumor Society.

Back pain, high blood pressure, stroke and brain tumor

For a year, a 51 year old male had been suffering from back pain.
This year, he suffered a stroke as a result of high blood pressure and the brain tumor that was discovered in the hospital when he was being treated for the stroke.

After the brain surgery (5 hours) where the brain tumor was removed by Stanford hospital doctors, the back pain went away. Before the stroke, he never took any anti-hypertensive medication and had been smoking since he was 19 yrs of age although he stopped heavy smoking during the past few years.

He led a sedentary lifestyle without exercise and stressful life. He is overweight by about 30lbs.
He called 911 before he had a stroke and right before he collapsed in front of the paramedics, he felt that something bad is going to happen to his body as he was feeling a stabbing knife on the top of his brain that flows to his back.

During the stroke episode after he called 911 himself, he was perspiring profusely like he was wet by a hose of water all over his body.
Now, thanks to the Stanford hospital doctors, he is back to work after spending 3.5 weeks in the hospital.

He now focus on spending quality time with his kids and is thankful to God for his second life. Since we work together in the same company, I am currently helping him with proper nutrition and lifestyle choices from food, walking after lunch hours, letting fresh air enter the house and his environment, stress-free lifestyle with gratitude and positive spirit and many other healing ways.