Saturday, January 27, 2018

Hits, not concussions, cause CTE

It's Super Bowl week and America turns its eyes to the biggest event of the year. America loves its football. But will the game survive the concussion/CTE crisis affecting those who play the game?


New insights into the disease show head impact, not concussion, triggers CTE and pave way for early detection, prevention and treatment January 18, 2018 Boston University School of Medicine Researchers have identified evidence of early Chronic Traumatic Encephalopathy (CTE) brain pathology after head impact ­­ even in the absence of signs of concussion.


Early indicators of CTE pathology not only persisted long after injury but also spread through the brain, providing the best evidence to date that head impact, not concussion, causes CTE.

Researchers have identified evidence of early Chronic Traumatic Encephalopathy (CTE) brain pathology after head impact ­­ even in the absence of signs of concussion. Early indicators of CTE pathology not only persisted long after injury but also spread through the brain, providing the best evidence to date that head impact, not concussion, causes CTE.

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The findings, published online in the journal Brain, are based on analysis of human brains from teenagers with recent head injury and mouse models that recreate sports­related head impact and military­related blast exposure. The investigators also performed laboratory experiments and computer modeling. Study results shed light on the origins of CTE and relationship to traumatic brain injury (TBI), concussion and subconcussive head injury. CTE is a neurodegenerative disease characterized by abnormal accumulation of tau protein around small blood vessels in the brain. CTE causes brain cell death, cognitive deficits, and dementia. The brain pathology of CTE has been observed in brains of teenagers and adults with exposure to repeated head injury, both concussive and subconcussive episodes. However, the mechanisms that cause CTE and relationship to concussion, subconcussive injury and TBI remain poorly understood. In the first part of their study, the researchers examined four postmortem brains from teenage athletes who had sustained closed­head impact injuries 1, 2, 10 and 128 days prior to death. Neuropathological analysis of these brains showed a spectrum of post­traumatic pathology, including one case of earlystage CTE and two cases with abnormal accumulation of tau protein. Brains from four age­matched athletes without recent head injury did not show the pathological changes observed in the head­injury group.

To investigate causal mechanisms underlying these changes, the researchers conducted laboratory experiments using mouse models of two different injury mechanisms ­­ repeat closed­head impact and blast exposure ­­ both linked to CTE. The investigators compared brain responses to the experimental injuries and relationship to CTE pathology over time. Based on pathological findings in human cases, the researchers hypothesized that early CTE may result from damaged blood vessels in the brain that become leaky, resulting in blood proteins spilling into brain tissue and triggering brain inflammation. The researchers utilized a brain scan called dynamic contrastenhanced magnetic resonance imaging (DCE­MRI) to detect leaky blood vessels in the brains of mice subjected to head impact.


The investigators also found that head impact caused persistent changes in brain electrical functions, which may explain cognitive difficulties experienced by some people after these injuries. "The same brain pathology that we observed in teenagers after head injury was also present in headinjured mice. We were surprised that the brain pathology was unrelated to signs of concussion, including altered arousal and impaired balance, among others. Our findings provide strong causal evidence linking head impact to TBI and early CTE, independent of concussion," explained corresponding author Lee E. Goldstein, MD, PhD, an associate professor at Boston University School of Medicine and College of Engineering. "The results may explain why approximately 20 percent of athletes with CTE never suffered a diagnosed concussion."

Source: ScienceDaily, Boston University

Wednesday, January 24, 2018

Parkinson's: What Neil Diamond (and millions) face




Parkinson's disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. The four primary symptoms of PD are tremor, or trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks. PD usually affects people over the age of 60.  Early symptoms of PD are subtle and occur gradually.  In some people the disease progresses more quickly than in others.  As the disease progresses, the shaking, or tremor, which affects the majority of people with PD may begin to interfere with daily activities. 

At present, there is no cure for PD, but a variety of medications provide dramatic relief from the symptoms.  Usually, affected individuals are given levodopa combined with carbidopa.  Carbidopa delays the conversion of levodopa into dopamine until it reaches the brain.  Nerve cells can use levodopa to make dopamine and replenish the brain's dwindling supply.  Although levodopa helps at least three-quarters of parkinsonian cases, not all symptoms respond equally to the drug. Bradykinesia and rigidity respond best, while tremor may be only marginally reduced. Problems with balance and other symptoms may not be alleviated at all.  Anticholinergics may help control tremor and rigidity.  Other drugs, such as bromocriptine, pramipexole, and ropinirole, mimic the role of dopamine in the brain, causing the neurons to react as they would to dopamine. 

PD is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time.  Although some people become severely disabled, others experience only minor motor disruptions. Tremor is the major symptom for some individuals, while for others tremor is only a minor complaint and other symptoms are more troublesome.  It is currently not possible to predict which symptoms will affect an individual, and the intensity of the symptoms also varies from person to person.

Source: NINDS/NIH

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Saturday, January 13, 2018

Fear in Hawaii: The Biology of Stress




Residents and visitors in Hawaii were sent into a panic after officials accidentally sent an emergency alert warning of a "ballistic missile threat." It took officials 30 minutes to send a correction.


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From Healing the Brain: "Wounds that Time Alone Won’t Heal The Biology of Stress."

Imagine you are a zebra grazing on the plains of Africa. It's midday. The sun is bright, the food is plentiful.

Suddenly you sense an attack. A lion is chasing you. Its fight or flight in action.

Your brain tells your body to prepare for a fight or take flight. The body responds by preparing extra hormones to create more energy and by increasing the rate the heart pumps blood to the muscles. For most animals, this stress reaction lasts for just a short time and it saves lives.  

As a body is preparing for fight or flight, however, practically all systems, such as digestion, physical growth, and warding off diseases are placed on hold. This means that people for whom stress has become a way of life are endangering their overall health. Researchers have learned by studying primates whose systems are similar to human beings that those who learn to have control over their lives and are able to reduce or avoid stress live longer and healthier lives.

Are zebras better equipped to deal with stress than humans? No. However, according to Dr. Robert Sapolsky, author of ​Why Zebras Don't Get Ulcers, "For a zebra, stress is three minutes of some screaming terror running from a lion. After the chase, either it's over or they are." On the other hand humans, he says, have constructed a network of social stressors. Since we are obliged to live in this framework, stress builds up.

How do the brain and the body react to stress? Stress, such as the threat of attack, forces various changes in the body. First, adrenaline causes an increase in heart rate and blood pressure so that blood can be sent to muscles faster. Second, the brain’s hypothalamus signals the pituitary gland to stimulate the adrenal gland (specifically the adrenal cortex) to produce cortisol.

This stress hormone, a longer-acting steroid, helps the body to mobilize energy. However, prolonged exposure to cortisol can damage virtually every part of the body. Chronic high blood pressure can cause blood vessel damage and the long-term shutdown of digestion can lead to ulcers.  

Thursday, January 4, 2018

Real hope for Alzheimer's

A drug developed for diabetes could be used to treat Alzheimer's


A drug developed for diabetes could be used to treat Alzheimer's after scientists found it 'significantly reversed memory loss' in mice through a triple method of action. This is the first time that a triple receptor drug has been used which acts in multiple ways to protect the brain from degeneration. It combines three growth factors. Problems with growth factor signalling have been shown to be impaired in the brains of Alzheimer's patients.





A drug developed for diabetes could be used to treat Alzheimer's after scientists found it "significantly reversed memory loss" in mice through a triple method of action.
The research, published in Brain Research, could bring substantial improvements in the treatment of Alzheimer's disease through the use of a drug originally created to treat type 2 diabetes.

Lead researcher Professor Christian Holscher of Lancaster University in the UK said the novel treatment "holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer's disease."

Alzheimer's disease is the most common cause of dementia and the numbers are expected to rise to two million people in the UK by 2051 according to Alzheimer's Society, who part- funded the research.

Dr. Doug Brown, Director of Research and Development at Alzheimer's Society, said: "With no new treatments in nearly 15 years, we need to find new ways of tackling Alzheimer's. It's imperative that we explore whether drugs developed to treat other conditions can benefit people with Alzheimer's and other forms of dementia. This approach to research could make it much quicker to get promising new drugs to the people who need them."

Although the benefits of these 'triple agonist' drugs have so far only been found in mice, other studies with existing diabetes drugs such as liraglutide have shown real promise for people with Alzheimer's, so further development of this work is crucial."

This is the first time that a triple receptor drug has been used which acts in multiple ways to protect the brain from degeneration. It combines GLP-1, GIP and Glucagon which are all growth factors. Problems with growth factor signalling have been shown to be impaired in the brains of Alzheimer's patients.
The study used APP/PS1 mice, which are transgenic mice that express human mutated genes that cause Alzheimer's. Those genes have been found in people who have a form of Alzheimer's that can be inherited. Aged transgenic mice in the advanced stages of neurodegeneration were treated.
In a maze test, learning and memory formation were much improved by the drug which also:-
  • enhanced levels of a brain growth factor which protects nerve cell functioning
  • reduced the amount of amyloid plaques in the brain linked with Alzheimer's
  • reduced both chronic inflammation and oxidative stress
  • slowed down the rate of nerve cell loss
Professor Holscher said: "These very promising outcomes demonstrate the efficacy of these novel multiple receptor drugs that originally were developed to treat type 2 diabetes but have shown consistent neuro- protective effects in several studies."

"Clinical studies with an older version of this drug type already showed very promising results in people with Alzheimer's disease or with mood disorders"

"Here we show that a novel triple receptor drug shows promise as a potential treatment for Alzheimer's but further dose-response tests and direct comparisons with other drugs have to be conducted in order to evaluate if this new drugs is superior to previous ones."

Type 2 diabetes is a risk factor for Alzheimer's and has been implicated in the progression of the disease. Impaired insulin has been linked to cerebral degenerative processes in type 2 diabetes and Alzheimer's disease. Insulin desensitisation has also been observed in the Alzheimer's disease brain. The desensitisation could play a role in the development of neurodegenerative disorders as insulin is a growth factor with neuroprotective properties.

Monday, January 1, 2018

Marijuana 101 for 2018



As of 2018, California joins the growing list of states to allow recreational use of marijuana. What hasn't changed is the drug and how it works.

When marijuana is smoked or vaporized, THC quickly passes from the lungs into the bloodstream, which carries it to organs throughout the body, including the brain. Its effects begin almost immediately and can last from 1 to 3 hours. Decision making, concentration, and memory can be affected for days after use, especially in regular users. If marijuana is consumed in foods or beverages, the effects of THC appear later—usually in 30 minutes to 1 hour—and may last for many hours.
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As it enters the brain, THC attaches to cells, or neurons, with specific kinds of receptors called cannabinoid receptors. Normally, these receptors are activated by chemicals similar to THC that occur naturally in the body. They are part of a communication network in the brain called the endocannabinoid system. This system is important in normal brain development and function.
Marijuana's Effects on the Brain
Most of the cannabinoid receptors are found in parts of the brain that influence pleasure, memory, thinking, concentration, sensory and time perception, and coordinated movement. Marijuana activates the endocannabinoid system, which causes the pleasurable feelings or "high" and stimulates the release of dopamine in the brain's reward centers, reinforcing the behavior. Other effects include changes in perceptions and mood, lack of coordination, difficulty with thinking and problem solving, and disrupted learning and memory.
Certain parts of the brain have a lot of cannabinoid receptors. These areas are the hippocampus, the cerebellum, the basal ganglia, and the cerebral cortex. As a result, marijuana affects these functions: 
  • Learning and memory. The hippocampus plays a critical role in certain types of learning. Disrupting its normal functioning can lead to problems studying, learning new things, and recalling recent events. Chronic marijuaua use disorder, that begins in adolescence, is associated with a loss of IQ points, as compared with people who don't use marijuana during their teen years. However, two recent twin studies suggest that this decline is related to other risk factors (e.g., genetics, family, and environment), not by marijuana use itself.
  • Coordination. THC affects the cerebellum, the area of our brain that controls balance and coordination, and the basal ganglia, another part of the brain that helps control movement. These effects can influence performance in such activities as sports, driving, and video games.
  • Judgment. Since THC affects areas of the frontal cortex involved in decision making, using it can make you more likely to engage in risky behavior, such as unprotected sex or getting in a car with someone who’s been drinking or is high on marijuana.
Learn more about how the brain works and what happens when a person uses drugs. And, check out how the brain responds to marijuana.

Source: NIDA/NIH