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

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

Learn more about your brain, here.

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.

What happens in your brain...in clear, concise language.

What could people have been feeling?

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.  

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.

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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.

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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.

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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.

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.

Learn about the brain and behavior in clear language. Click here.

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.

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

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For New Year's Eve: Impaired Driving 911

Use of illicit* drugs or misuse of prescription drugs can make driving a car unsafe—just like driving after drinking alcohol. Drugged driving puts the driver, passengers, and others who share the road at risk.

Why is drugged driving dangerous? The effects of specific drugs differ depending on how they act in the brain. For example, marijuana can slow reaction time, impair judgment of time and distance, and decrease coordination. Drivers who have used cocaine or methamphetamine can be aggressive and reckless when driving. Certain kinds of sedatives, called benzodiazepines, can cause dizziness and drowsiness.

Get the facts on drugs and the brain.

All of these impairments can lead to vehicle crashes. Research studies have shown negative effects of marijuana on drivers, including an increase in crashes. Which drugs are linked to drugged driving? After alcohol, marijuana is the drug most often found in the blood of drivers involved in crashes.

Tests for detecting marijuana in drivers measure the level of delta­9­ tetrahydrocannabinol (THC), marijuana’s mind­altering ingredient, in the blood. But the role that marijuana plays in crashes is often unclear. THC can be detected in body fluids for days or even weeks after use, and it is often combined with alcohol. The risk associated with marijuana in combination with alcohol, cocaine, or benzodiazepines appears to be greater than that for either drug by itself.

Several studies have shown that drivers with THC in their blood were roughly twice as likely to be responsible for a deadly crash or be killed than drivers who hadn't used drugs or alcohol. However, a large NHTSA study found no significant increased crash risk traceable to marijuana after controlling for drivers’ age, gender, race, and presence of alcohol. More research is needed.

Along with marijuana, prescription drugs are also commonly linked to drugged driving crashes. A 2010 nationwide study of deadly crashes found that about 47 percent of drivers who tested positive for drugs had used a prescription drug, compared to 37 percent of those had used marijuana and about 10 percent of those who had used cocaine. The most common prescription drugs found were pain relievers. However, the study didn't distinguish between medicallysupervised and illicit use of the prescription drugs.

How often does drugged driving cause crashes? It's hard to measure how many crashes are caused by drugged driving. This is because: a good roadside test for drug levels in the body doesn't yet exist police don't usually test for drugs if drivers have reached an illegal blood alcohol level because there's already enough evidence for a DUI charge many drivers who cause crashes are found to have both drugs and alcohol or more than one drug in their system, making it hard to know which substance had the greater effect.

One NHTSA study found that in 2009, 18 percent of drivers killed in a crash tested positive for at least one drug. A 2010 study showed that 11 percent of deadly crashes involved a drugged driver.

Why is drugged driving a problem in teens and young adults? Teen drivers are less experienced and are more likely than older drivers to underestimate or not recognize dangerous situations. They are also more likely to speed and allow less distance between vehicles. When lack of driving experience is combined with drug use, the results can be tragic. Car crashes are the leading cause of death among young people aged 16 to 19 years.

A 2011 survey of middle and high school students showed that, in the 2 weeks before the survey, 12 percent of high school seniors had driven after using marijuana, compared to around 10. Drugged Driving in Older Adults In 2010, more than one­quarter of drugged drivers in deadly crashes were aged 50 years or older. Illicit drug use in adults aged 50 to 59 has increased, more than doubling from 3 percent in 2002 to 7 percent in 2010. Mental decline in older adults can lead to taking a prescription drug more or less often than they should or in the wrong amount. Older adults also may not break down the drug in their system as quickly as younger people. These factors can lead to unintended intoxication while behind the wheel of a car.

A study of college students with access to a car found that 1 in 6 had driven under the influence of a drug other than alcohol at least once in the past year. Marijuana was the most common drug used, followed by cocaine and prescription pain relievers. What steps can people take to prevent drugged driving? Because drugged driving puts people at a higher risk for crashes, public health experts urge people who use drugs and alcohol to develop social strategies to prevent them from getting behind the wheel of a car while impaired. Steps people can take include: offering to be a designated driver appointing a designated driver to take all car keys getting a ride to and from parties where there are drugs and alcohol discussing the risks of drugged driving with friends in advance

In 2014, 10 million people aged 12 or older reported driving under the influence of illicit drugs in the past year. It's hard to measure how many crashes drugged driving causes. After alcohol, marijuana is the drug most often linked to drugged driving. In 2010, more than one­quarter of drugged drivers in fatal crashes were aged 50 years or older. When lack of driving experience is combined with drug use, the results can be tragic. People who use drugs and alcohol should develop social strategies to prevent them from getting behind the wheel of a car while impaired.

Source: National Institute on Drug Abuse.

Drug Abuse and LGBT Community: Social Anxiety on Steroids

People who identify as lesbian, gay, bisexual, or transgender (LGBT) often face social stigma, discrimination, and other challenges not encountered by people who identify as heterosexual. They also face a greater risk of harassment and violence. As a result of these and other stressors, sexual minorities are at increased risk for various behavioral health issues.

Many federally funded surveys have only recently started to ask about sexual orientation and gender identification in their data collections. Surveys thus far have found that sexual minorities have higher rates of substance misuse and substance use disorders (SUDs) than people who identify as heterosexual. Therefore, it is not yet possible to establish long-term trends about substance use and SUD prevalence in LGBT populations.

Substance Use and Misuse

Understand social anxiety and stress in the LGBT community.

According to 2015 data from the National Survey on Drug Use and Health, adults defined as "sexual minority" (in this survey, meaning lesbian, gay, or bisexual) were more than twice as likely as heterosexual adults (39.1 percent versus 17.1 percent) to have used any illicit drug in the past year. Nearly a third of sexual minority adults (30.7 percent) used marijuana in the past year, compared to 12.9 percent of heterosexual adults, and about 1 in 10 (10.4 percent) misused prescription pain relievers, compared to 4.5 percent of heterosexual adults.

A 2013 survey conducted by the U.S. Census Bureau found that a higher percentage of LGBT adults between 18 and 64 reported past-year binge drinking (five or more drinks on a single occasion) than heterosexual adults. LGBT people in treatment for SUDs initiated alcohol consumption earlier than their heterosexual counterparts.

Lesbian, gay, and bisexual (LGB) adolescents also reported higher rates of substance use compared to heterosexual adolescents. In one meta-analysis, LGB adolescents were 90 percent more likely to use substances than heterosexual adolescents, and the difference was particularly pronounced in some subpopulations; bisexual adolescents used substances at 3.4 times the rate of heterosexual adolescents, and lesbian and bisexual females used at four times the rate of their heterosexual counterparts.

Substance Use Disorders and Comorbidities

LGBT persons also have a greater likelihood than non-LGBT persons of experiencing a substance use disorder (SUD) in their lifetime, and they often enter treatment with more severe SUDs. Some common SUD treatment modalities have been shown to be effective for gay or bisexual men including motivational interviewing, social support therapy, contingency management, and cognitive-behavioral therapy (CBT).

Addiction treatment programs offering specialized groups for gay and bisexual men showed better outcomes for those clients compared to gay and bisexual men in non-specialized programs; but in one study, only 7.4 percent of programs offered specialized services for LGBT patients. Research is currently limited on rates of SUD among transgender populations, although research shows that transgender individuals are more likely to seek SUD treatment than the non-transgender population. Current research suggests that treatment should address unique factors in these patients' lives that may include homophobia/transphobia, family problems, violence, and social isolation.

Sexual minorities with SUDs are more likely to have additional (comorbid or co-occurring) psychiatric disorders. For example, gay and bisexual men and lesbian and bisexual women report greater odds of frequent mental distress and depression than their heterosexual counterparts. Transgender children and adolescents have higher levels of depression, suicidality, self-harm, and eating disorders than their non-transgender counterparts.Thus it is particularly important that LGBT people in SUD treatment be screened for other psychiatric problems (as well as vice versa) and all identifiable conditions should be treated concurrently.

LGBT people are also at increased risks for human immunodeficiency virus (HIV) due to both intravenous drug use and risky sexual behaviors. HIV infection is particularly prevalent among gay and bisexual men (men who have sex with men, or MSM) and transgender women who have sex with men. SUD treatment can also help prevent HIV transmission among those at high risk. For example, addiction treatment is associated not only with reduced drug use but also with less risky sexual behavior among MSM, and those with HIV report improvements in viral load.

Source: National Institute on Drug Abuse