No link found between youth contact sports and cognitive, mental health problems
October 21, 2019
Science Daily/University of Colorado at Boulder
Adolescents who play contact sports, including football, are no more likely to experience cognitive impairment, depression or suicidal thoughts in early adulthood than their peers, suggests a new University of Colorado Boulder study of nearly 11,000 youth followed for 14 years.
The study, published this month in the Orthopaedic Journal of Sports Medicine, also found that those who play sports are less likely to suffer from mental health issues by their late 20s to early 30s.
"There is a common perception that there's a direct causal link between youth contact sports, head injuries and downstream adverse effects like impaired cognitive ability and mental health," said lead author Adam Bohr, PhD, a postdoctoral researcher in the Department of Integrative Physiology. "We did not find that."
The study comes on the heels of several highly-publicized papers linking sport-related concussion among former professional football players to chronic traumatic encephalopathy (CTE), cognitive decline and mental health issues later in life. Such reports have led many to question the safety of youth tackle football, and participation is declining nationally.
But few studies have looked specifically at adolescent participation in contact sports.
"When people talk about NFL players, they are talking about an elite subset of the population," said senior author Matthew McQueen, an associate professor of integrative physiology. "We wanted to look specifically at kids and determine if there are true harms that are showing up early in adulthood."
The study analyzed data from 10,951 participants in the National Longitudinal Study of Adolescent to Adult Health (Add Health), a representative sample of youth in seventh through 12th grades who have been interviewed and tested repeatedly since 1994.
Participants were categorized into groups: those who, in 1994, said they intended to participate in contact sports; those who intended to play non-contact sports; and those who did not intend to play sports. Among males, 26% said they intended to play football.
After controlling for socioeconomic status, education, race and other factors, the researchers analyzed scores through 2008 on word and number recall and questionnaires asking whether participants had been diagnosed with depression or attempted or thought about suicide.
"We were unable to find any meaningful difference between individuals who participated in contact sports and those who participated in non-contact sports. Across the board, across all measures, they looked more or less the same later in life," said Bohr.
Football players -- for reasons that are not clear -- actually had a lower incidence of depression in early adulthood than other groups.
Those who reported they did not intend to participate in sports at age 8 to 14 were 22% more likely to suffer depression in their late 20s and 30s.
"Right now, football is in many ways being compared to cigarette smoking -- no benefit and all harm," said McQueen, who is also director for the Pac-12 Concussion Coordinating Unit. "It is absolutely true that there is a subset of NFL players who have experienced horrible neurological decline, and we need to continue to research to improve our understanding of that important issue."
But, he said, "the idea that playing football in high school will lead to similar outcomes later in life as those who played in the NFL is not consistent with the evidence. In fact, we and others have found there is some benefit to playing youth sports."
A recent University of Pennsylvania study of 3,000 men who had graduated high school in Wisconsin in 1957 found that those who played football were no more likely to suffer depression or cognitive impairment later. But some pointed out that the sport had changed radically since the 1950s.
The new study is among the largest to date and looks at those who played football in the 1990s.
The authors note that, due to the design of the dataset, they were only able to measure "intended" participation. (Due to the timing of the questionnaires, however, it is likely that those who reported participation in football actually did participate.)
They also could not tell how long an adolescent played, what position or whether a concussion or sub-concussive head injury was ever sustained. Further studies should be done exploring those factors, they said.
"Few current public health issues are as contentious and controversial as the safety and consequences of participation in football," they concluded. "Research on the risks of participation weighed with the risks of not participating in sports will enable parents and young athletes to make educated, informed decisions based on solid evidence."
A new CU Boulder study, looking at the long-term mental and physical health of CU student-athlete alumni, is already underway.
https://www.sciencedaily.com/releases/2019/10/191021082749.htm
A new culprit in cognitive decline in Alzheimer's disease
Study finds blood protein destroys memory storage sites in the brain and may lead to new treatments
February 5, 2019
Science Daily/Gladstone Institutes
Scientists have shown for the first time that a blood-clotting protein called fibrinogen is responsible for a series of molecular and cellular events that can destroy connections between neurons in the brain and result in cognitive decline.
It has long been known that patients with Alzheimer's disease have abnormalities in the vast network of blood vessels in the brain. Some of these alterations may also contribute to age-related cognitive decline in people without dementia. However, the ways in which such vascular pathologies contribute to cognitive dysfunction have largely remained a mystery. Until now, that is.
Scientists at the Gladstone Institutes, led by Senior Investigator Katerina Akassoglou, PhD, showed for the first time that a blood-clotting protein called fibrinogen is responsible for a series of molecular and cellular events that can destroy connections between neurons in the brain and result in cognitive decline.
Akassoglou and her team used state-of-the-art imaging technology to study both mouse brains and human brains from patients with Alzheimer's disease. They also produced the first three-dimensional volume imaging showing that blood-brain barrier leaks occur in Alzheimer's disease.
In their study, published in the scientific journal Neuron, the researchers found that fibrinogen, after leaking from the blood into the brain, activates the brain's immune cells and triggers them to destroy important connections between neurons. These connections, called synapses, are critical for neurons to communicate with one another.
Previous studies have shown that elimination of synapses causes memory loss, a common feature in Alzheimer's disease and other dementias. Indeed, the scientists showed that preventing fibrinogen from activating the brain's immune cells protected mouse models of Alzheimer's disease from memory loss.
"We found that blood leaks in the brain can cause elimination of neuronal connections that are important for memory functions," explains Akassoglou, who is also a professor of neurology at UC San Francisco (UCSF). "This could change the way we think about the cause and possible cure of cognitive decline in Alzheimer's disease and other neurological diseases."
The team showed that fibrinogen can have this effect even in brains that lack amyloid plaques, which are the focus of diverse treatment strategies that have failed in large clinical trials. The researchers showed that injecting even extremely small quantities of fibrinogen into a healthy brain caused the same kind of immune cell activation and loss of synapses they saw in Alzheimer's disease.
"Traditionally, the build-up of amyloid plaques in the brain has been seen as the root of memory loss and cognitive decline in Alzheimer's disease," says Mario Merlini, first author of the study and a staff research scientist in Akassoglou's laboratory at Gladstone. "Our work identifies an alternative culprit that could be responsible for the destruction of synapses."
The scientists' data help explain findings from recent human studies in which elderly people with vascular pathology showed similar rates of cognitive decline as age-matched people with amyloid pathology. However, patients with both types of pathology had much worse and more rapid cognitive decline. Other studies also identified vascular pathology as a strong predictor of cognitive decline that can act independently of amyloid pathology.
"Given the human data showing that vascular changes are early and additive to amyloid, a conclusion from those studies is that vascular changes may have to be targeted with separate therapies if we want to ensure maximum protection against the destruction of neuronal connections that leads to cognitive decline," says Akassoglou.
Interestingly, Akassoglou and her colleagues recently developed an antibody that blocks the interaction between fibrinogen and a molecule on the brain's immune cells. In a previous study, they showed this antibody protected mouse models of Alzheimer's disease from brain inflammation and neuronal damage.
"These exciting findings greatly advance our understanding of the contributions that vascular pathology and brain inflammation make to the progression of Alzheimer's disease," said Lennart Mucke, MD, co-author of the study and director of the Gladstone Institute of Neurological Disease. "The mechanisms our study identified may also be at work in a range of other diseases that combine leaks in the blood-brain barrier with neurological decline, including multiple sclerosis, traumatic brain injury, and chronic traumatic encephalopathy. It has far-reaching therapeutic implications."
https://www.sciencedaily.com/releases/2019/02/190205115419.htm
Antioxidant therapy may have promising potential in concussion treatment
April 1, 2015
Federation of American Societies for Experimental Biology (FASEB)
Antioxidants may play a key role in reducing the long-term effects of concussions and could potentially offer a unique new approach for treatment, a new study suggests. Common among athletes and soldiers, it is estimated that 3.4 million concussions occur each year in the United States. The development of a readily available oral supplement would have the potential to improve brain function in a percentage of concussion sufferers.
Common among athletes and soldiers, it is estimated that 3.4 million concussions occur each year in the United States. The development of a readily available oral supplement would have the potential to improve brain function in a percentage of concussion sufferers.
The study adds to recent findings that concussions can lead to chronic traumatic encephalopathy. Head injuries often lead to chronic traumatic encephalopathy, a disease associated with long-term brain damage and behavioral symptoms including memory loss, impulsive behavior, depression and aggression. The number of retired athletes and veterans diagnosed with chronic traumatic encephalopathy has climbed in recent years.
"Concussions can contribute to long-term changes within the brain and these changes are the result of cell death, which may be caused by oxidative stress," said Brandon Lucke-Wold, a M.D./Ph.D. student at West Virginia University's Medical School who conducted the research. "This study shows that antioxidants such as lipoic acid can reduce the long-term deficits when given after a concussion."
In Lucke-Wold's research, rats were divided into three groups: a non-concussed control group, a group that experienced concussive injury and another concussed group that received lipoic acid supplementation. Seven days after the concussion, the rats were tested for seemingly impulsive behavior through an elevated maze. The rats exposed to concussion without lipoic acid had increased impulsive behavior, and spent more time exploring open spaces indicative of risk taking behavior.
"This increase in impulsive behavior was an indication of underlying brain damage," said Lucke-Wold, who will present the research at the American Society for Pharmacology and Experimental Therapeutics (ASPET) Annual Meeting during Experimental Biology 2015.
Analysis of brains of the group receiving supplementation showed markedly decreased impulsive behavior. "These findings make sense because lipoic acid works to help reduce toxic free radicals that can damage cells," said Lucke-Wold.
"By understanding the mechanisms behind brain injury following concussion, we can more effectively target treatment interventions to reduce these damaging effects," he added.
http://www.sciencedaily.com/releases/2015/04/150401132752.htm
Call for more research on brain damage in American football
March 24, 2015
Science Daily/BMJ
More research is needed to identify how athletes sustain brain injury from American football, and also to develop strategies to protect them, write experts. Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome that can affect athletes. It is thought to result from concussion and brain injury following repeated blows to the head.
But the topic of brain damage in football is controversial. The National Football League, for example, does not acknowledge any association between football and brain injury.
CTE symptoms include memory problems, depression, poor impulse and motor control, anger and apathy. But diagnosis can be confirmed only with an autopsy.
Over the course of the last 60 years, just 63 cases of CTE have been identified. When compared to the millions of football players, this number is very low, explain the authors, and this makes research "challenging" as definitive conclusions are difficult to make based on small samples.
Consequently, it will take time and further research to make American football safer, but it must remain a top priority, they argue.
All cases of confirmed CTE following autopsy suggest that the condition is linked to repetitive blows to the head.
But not all of these persons had a history of concussion and this suggests that undiagnosed subconcussive blows may also contribute to CTE, they explain, and call for more research into how the condition develops and to determine other risk factors.
Previous research has shown that retired NFL players demonstrated more cognitive impairment if they had started playing football at a younger age, and this suggests the role of long term injuries to the head.
The development of new technologies that can measure subconcussive blows would benefit research, add the authors. For example, helmet mounted accelerometers can measure these blows and has shown that high school players can sustain over 1,000 head impacts per season. But the NFL recently stopped its use because of difficulties and questions over the reliability of such data.
Risk reduction of head injuries has included legislation requiring injured athletes to be medically assessed before returning to play and changing rules to avoid or reduce head trauma. But long term studies still need to assess whether these strategies are effective, they add.
Protective equipment, such as helmets, have been implemented, but have mixed results and more mechanisms to reduce trauma and to treat injuries should be developed and evaluated, they argue.
"We are still lacking a clear clinical picture because there have been no long term prospective studies of the disease spectrum from diagnosis to death," write the authors. "It is unclear whether any treatment could slow progression of the disease if it was recognised early."
http://www.sciencedaily.com/releases/2015/03/150324210049.htm