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Summary: A new study from researchers at Boston University reports an increase in later life emotional and behavioral problems in people who played youth tackle football before the age of 12.

Source: Boston University School of Medicine.

A new study has found an association between participation in youth tackle football before age 12 and impaired mood and behavior later in life. The study appears in Nature’s Translational Psychiatry.

Researchers from Boston University’s Chronic Traumatic Encephalopathy (CTE) Center studied 214 former American football players, including 43 who played only through high school and 103 who played only through college. The average age of the former players at the time of the study was 51. Participants received telephone-administered cognitive tests and completed online measures of depression, behavioral regulation, apathy and executive functioning (initiating activity, problem-solving, planning and organization). Results from former players who started playing tackle football before the age of 12 were compared against those of participants who started playing at age 12 or later.

The study showed that participation in youth football before age 12 increased the risk of problems with behavioral regulation, apathy and executive functioning by two-fold and increased the risk of clinically elevated depression scores by three-fold. The increased risk was independent of the total number of years the participants played football, the number of concussions they reported, or whether they played through high school, college or professionally. The researchers chose the cutoff of age 12 because the brain undergoes a key period of development and maturation between the years 10-12 in males. They examined other age cutoffs as well, though the age 12 cutoff led to the most robust findings. In addition, even when a specific age cutoff was not used, younger age of first exposure to football was associated with worse clinical function.

The new study follows previous research from the BU CTE Center that examined former professional players. In those studies, the former NFL players who started tackle football prior to age 12 had worse memory and mental flexibility, as well as structural brain changes on MRI scans, compared to former players who began at age 12 or older.

“This study adds to growing research suggesting that incurring repeated head impacts through tackle football before the age of 12 can lead to a greater risk for short- and long-term neurological consequences,” said Michael Alosco, PhD, lead author of the study and a post-doctoral fellow at Boston University School of Medicine (BUSM).

However, more research on this topic is needed before any recommendations on policy or rule changes can be made,” stated corresponding author Robert Stern, PhD, professor of neurology, neurosurgery and anatomy and neurobiology at BUSM.

The researchers point out there are many important health and psychosocial benefits of participating in athletics and team sports during pre-adolescence.

Researchers from the University of Wisconsin-Madison and Harvard University also participated in this study.

Funding: This work was supported by grants from the National Institutes of Health (NIH; R01 NS 078337; R56 9500304025; U01 NS093334; U01NS086659-01; K23AG046377). This publication also was supported by the National Center for Advancing Translational Sciences, NIH, through BUCTSI Grant Number 1UL1TR001430, as well as the Concussion Legacy Foundation. Michael L. Alosco and research reported in this publication are supported by a Pilot Grant from the Boston University Alzheimer’s Disease Center (AG013846), and NIH/NINDS under grant number F32NS096803.

Source: Gina DiGravio – Boston University School of Medicine
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Age of first exposure to American football and long-term neuropsychiatric and cognitive outcomes” by M L Alosco, A B Kasimis, J M Stamm, A S Chua, C M Baugh, D H Daneshvar, C A Robbins, M Mariani, J Hayden, S Conneely, R Au, A Torres, M D McClean, A C McKee, R C Cantu, J Mez, C J Nowinski, B M Martin, C E Chaisson, Y Tripodis & R A Stern in Translational Psychiatry. Published online September 19 2017 doi:10.1038/tp.2017.197

Abstract

Age of first exposure to American football and long-term neuropsychiatric and cognitive outcomes

Previous research suggests that age of first exposure (AFE) to football before age 12 may have long-term clinical implications; however, this relationship has only been examined in small samples of former professional football players. We examined the association between AFE to football and behavior, mood and cognition in a large cohort of former amateur and professional football players. The sample included 214 former football players without other contact sport history. Participants completed the Brief Test of Adult Cognition by Telephone (BTACT), and self-reported measures of executive function and behavioral regulation (Behavior Rating Inventory of Executive Function-Adult Version Metacognition Index (MI), Behavioral Regulation Index (BRI)), depression (Center for Epidemiologic Studies Depression Scale (CES-D)) and apathy (Apathy Evaluation Scale (AES)). Outcomes were continuous and dichotomized as clinically impaired. AFE was dichotomized into <12 and greater than or equal to12, and examined continuously. Multivariate mixed-effect regressions controlling for age, education and duration of play showed AFE to football before age 12 corresponded with >2 × increased odds for clinically impaired scores on all measures but BTACT: (odds ratio (OR), 95% confidence interval (CI): BRI, 2.16,1.19–3.91; MI, 2.10,1.17–3.76; CES-D, 3.08,1.65–5.76; AES, 2.39,1.32–4.32). Younger AFE predicted increased odds for clinical impairment on the AES (OR, 95% CI: 0.86, 0.76–0.97) and CES-D (OR, 95% CI: 0.85, 0.74–0.97). There was no interaction between AFE and highest level of play. Younger AFE to football, before age 12 in particular, was associated with increased odds for impairment in self-reported neuropsychiatric and executive function in 214 former American football players. Longitudinal studies will inform youth football policy and safety decisions.

“Age of first exposure to American football and long-term neuropsychiatric and cognitive outcomes” by M L Alosco, A B Kasimis, J M Stamm, A S Chua, C M Baugh, D H Daneshvar, C A Robbins, M Mariani, J Hayden, S Conneely, R Au, A Torres, M D McClean, A C McKee, R C Cantu, J Mez, C J Nowinski, B M Martin, C E Chaisson, Y Tripodis & R A Stern in Translational Psychiatry. Published online September 19 2017 doi:10.1038/tp.2017.197

A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria – are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.

This major call for action is based on substantial published evidence into Alzheimer’s. The team’s landmark editorial summarises the abundant data implicating these microbes, but until now this work has been largely ignored or dismissed as controversial – despite the absence of evidence to the contrary. Therefore, proposals for the funding of clinical trials have been refused, despite the fact that over 400 unsuccessful clinical trials for Alzheimer’s based on other concepts were carried out over a recent 10-year period.

Opposition to the microbial concepts resembles the fierce resistance to studies some years ago which showed that viruses cause certain types of cancer, and that a bacterium causes stomach ulcers. Those concepts were ultimately proved valid, leading to successful clinical trials and the subsequent development of appropriate treatments.

Professor Douglas Kell of The University of Manchester’s School of Chemistry and Manchester Institute of Biotechnology is one of the editorial’s authors. He says that supposedly sterile red blood cells were seen to contain dormant microbes, which also has implications for blood transfusions.

“We are saying there is incontrovertible evidence that Alzheimer’s Disease has a dormant microbial component, and that this can be woken up by iron dysregulation. Removing this iron will slow down or prevent cognitive degeneration – we can’t keep ignoring all of the evidence,” Professor Douglas Kell said.

Professor Resia Pretorius of the University of Pretoria, who worked with Douglas Kell on the editorial, said “The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease – particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation.”

The findings of this editorial could also have implications for the future treatment of Parkinson’s Disease, and other progressive neurological conditions.

Source: University of Manchester
Image Credit: The image is adapted from the University of Manchester press release.
Original Research: Full open access editorial for “Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152

Abstract

Microbes and Alzheimer’s Disease

We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.

AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic

“Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152

Summary: According to a new study, while brain regions that control sexual and aggressive behaviors in male and female mice are the same, the way they are wired is different.

Source: NYU School of Medicine.

Brain structures that control sexual and aggressive behavior in mice are wired differently in females than in males. This the finding of a study led by scientists at NYU School of Medicine and published online Sept. 18 in Nature Neuroscience.

Specifically, researchers found that, while control of aggressive behavior resides in same brain region in female and male mice, certain groups of brain cells in that region are organized differently. Two separate groups of cells were found to control sex and aggression in females, whereas circuits that encourage sex and aggression in males overlapped, say the study authors.

Knowing how aggressive behaviors are regulated is important because they are essential to survival in mice, as well as in humans, which have evolved to compete for food, mates, and territory, researchers say.

“Our study furthers our understanding of how these behaviors are organized differently in female and male mice brains,” says study senior investigator Dayu Lin, PhD, an assistant professor at the Neuroscience Institute at NYU Langone Health.

Having a detailed breakdown of brain functions by gender, Lin adds, is a “fundamental step” toward any future attempt to develop drugs that suppress extreme aggression in humans. She says research on female aggressive behavior has lagged because, in most animals, males are the more aggressive gender.

Original research by Lin and her team, published in Nature in 2011, was among the first to trace the origins of male aggression in mice to a distinct part of the hypothalamus, the brain region that controls body temperature, hunger, sleep, and levels of many hormones. This key part, the ventrolateral part of the ventromedial hypothalamus, or VMHvl, is located on the underside of the hypothalamus in mice and humans.

Other, recent studies that had blocked the action VMHvl cells in female mouse brains failed to trace the source of aggression control to the VMHvl. This blockade did stop all male and female attempts to mate, but did not reduce fighting among females, says Lin.

She says these other studies — having used a mouse type known for timidity — did not accurately replicate natural conditions. The current study was made more realistic by including a naturally aggressive mouse strain, as well as female virgin mice eager to fight off competitors for food, and new mothers anxious to protect their pups, say the authors.

The current study monitored the brain activity of the virgin and mother mice during fights with any female or male mouse that had entered their boxed space. The brains of all study mice were tested with electrical, genetic, or chemical probes that measured which nerve cells were turned on or off, and how this affected their fighting behavior. Researchers found that, under these more realistic conditions, turning VMHvl cells on or off did control whether female mice would fight. Researchers also monitored in males and females the activity of individual cells in the VMHvl with proteins that enable them to interact with the sex hormones (e.g. estrogen receptor alpha). Such cells had previously been linked to fighting behaviors in male mice.

Experiments showed that VMHvl cells actively transmitting signals, or “firing,” while females were mating were not the same cells firing when they were fighting. But in male mice, many of the same cells were firing during both activities. Further analysis showed that males had a mixed spatial distribution of the VMHvl cells involved in either behavior. In females, the cells involved in fighting were arranged along the center of the VMHvl, while those involved in mating were distributed along its borders.

Lin says her laboratory next plans to fine-tune tools for experimenting separately on the female mating and fighting VMHvl cells. She says her team also has plans to investigate the biological origins of these cells to determine how the female nerve circuity develops in contrast to the circuitry in males.

Funding: Funding support for the studies was provided by National Institute of Mental Health (NIMH) grants R01 MH101377 and R21 MH105774. Additional funding support was provided by the Mathers Foundation, Irma T. Hirschl Trust, Ester A. and Joseph Klingenstein Fund, Whitehall Foundation, Sloan Foundation, and McKnight Foundation.

Besides Lin, other NYU Langone scientists involved in this research were co-lead investigators Koichi Hashikawa, PhD, and Yoshiko Hashikawa, PhD; Robin Tremblay, PhD; James Feng, PhD; Alexander Sobol, PhD; Walter Piper, PhD; and Bernardo Rudy, MD, PhD. Additional research support was provided by Jiaxing Zhang, PhD, at Xiamen University in China; and by Hyosang Lee, PhD, at the Daegu Gyeongbuk Institute of Science and Technology in Korea.

Source: David March – NYU School of Medicine
Image Source: NeuroscienceNews.com image is credited to the researchers/Nature Neuroscience.
Original Research: Abstract for “Esr1+ cells in the ventromedial hypothalamus control female aggression” by Koichi Hashikawa, Yoshiko Hashikawa, Robin Tremblay, Jiaxing Zhang, James E Feng, Alexander Sabol, Walter T Piper, Hyosang Lee, Bernardo Rudy & Dayu Lin in Nature Neuroscience. Published online September 18 2017 doi:10.1038/nn.4644

Abstract

Esr1+ cells in the ventromedial hypothalamus control female aggression

As an essential means of resolving conflicts, aggression is expressed by both sexes but often at a higher level in males than in females. Recent studies suggest that cells in the ventrolateral part of the ventromedial hypothalamus (VMHvl) that express estrogen receptor-α (Esr1) and progesterone receptor are essential for male but not female mouse aggression. In contrast, here we show that VMHvlEsr1+ cells are indispensable for female aggression. This population was active when females attacked naturally. Inactivation of these cells reduced female aggression whereas their activation elicited attack. Additionally, we found that female VMHvl contains two anatomically distinguishable subdivisions that showed differential gene expression, projection and activation patterns after mating and fighting. These results support an essential role of the VMHvl in both male and female aggression and reveal the existence of two previously unappreciated subdivisions in the female VMHvl that are involved in distinct social behaviors.

“Esr1+ cells in the ventromedial hypothalamus control female aggression” by Koichi Hashikawa, Yoshiko Hashikawa, Robin Tremblay, Jiaxing Zhang, James E Feng, Alexander Sabol, Walter T Piper, Hyosang Lee, Bernardo Rudy & Dayu Lin in Nature Neuroscience. Published online September 18 2017 doi:10.1038/nn.4644

Summary: Researchers reveal a neuroendocrine system reflex may trigger an increased susceptibility to contracting bacterial infections following injuries to the brain or spinal cord.

Source: Charité.

A newly-discovered reflex arc mediates a process which leads to a disruption in the hormones secreted by the adrenal glands which, in turn, results in an increased susceptibility to bacterial infections. This research breaks new ground in the development of treatments to reduce the incidence of infections, and its results have been published in the current issue of Nature Neuroscience.

Injuries to the brain or spinal cord, such as those caused by stroke or trauma, result in a considerable weakening of the immune system. This often leads to severe infections, such as pneumonia or urinary tract infections, which hamper nervous tissue regeneration as well as rehabilitation in affected patients. Until now, our understanding of the exact manner in which nerve tissue damage leads to infections (and which physiological parameters are responsible) has remained rudimentary at best. Under the leadership of PD Dr. Harald Prüß (Charité’s Department of Neurology and the DZNE Berlin) and Prof. Dr. Dr. Jan M. Schwab (Head of Charité’s Department of Traumatic Spinal Cord Injuries), a team of researchers has now succeeded in deciphering this process.

“Our study was based on the premise that nerve pathways originating in the spinal cord exert a direct influence on organs involved in the immune system, such as lymph nodes and the spleen,” explains Dr. Prüß. He adds: “To our surprise, we found that the disruption of immune organ function does not occur as a result of this direct connection; instead, it is the result of an immune system dysregulation which affects the entire body.”

The researchers showed that the nervous system uses adrenal hormones as part of an indirect path of communication which results in the rapid breakdown of many immune cells. In a healthy body, the adrenal glands are controlled by both the nervous system and the relevant hormone control centers. Until recently, it had been assumed that a brain injury via hormonal signals results in the adrenal glands secreting cortisol, while a trauma-induced stress response results in the release of adrenaline and noradrenaline. “Our data show that the disruption in the normal function of the adrenal glands is under the direct control of damaged nerve tissue,” explains the neurologist. In contrast to received opinion, trauma-induced spinal cord injury initially resulted in a decrease in stress hormones and an increase in cortisol production.

This alteration in hormone levels led to a dramatic decrease in the numbers of many immune cells, particularly affecting the precursors of T-cells and B-cells. In some cases, this resulted in a reduction of between 50 and 80 percent in the size of the spleen, thymus or lymph nodes. While experimental deactivation of the adrenal glands led to a reversal of this dramatic loss of immune cells, the mice treated in this manner remained susceptible to infections. However, an autograft of adrenal tissue, transplanted into these mice, conferred protection against infections. While the transplanted adrenals produce the hormones needed by the body, they are no longer subject to the dysfunctional nervous system control mechanisms which develop following high level spinal injury.

The identification of this two-stage pathological reflex arc – consisting of nerve pathways between the spinal cord and the adrenal glands, as well as a hormone-mediated link with the immune system – helps to deepen our understanding of the interconnections which exist between the nervous and immune system. The discovery of this ‘immune system paralysis’ and its underlying mechanisms represents an important step on the path to improving the treatment of spinal cord injury patients. Rather than merely experiencing the more obvious symptom of motor-sensory paralysis, paraplegic patients also experience a paralysis of the immune system.

“Comprehensive analyses of patients’ cortisol and (nor)adrenaline levels have shown that they exhibit a fundamentally similar behavior to that seen in experimental studies,” explains Prof. Schwab. This suggests that treatment aimed at normalizing this neuro-endocrine reflex may prove effective in controlling the sometimes life-threatening infections associated with injuries to the central nervous system.

Source: Harald Prüss – Charité
Image Source: NeuroscienceNews.com image is credited to Harald Prüss.
Original Research: Abstract for “Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex” by Harald Prüss, Andrea Tedeschi, Aude Thiriot, Lydia Lynch, Scott M Loughhead, Susanne Stutte, Irina B Mazo, Marcel A Kopp, Benedikt Brommer, Christian Blex, Laura-Christin Geurtz, Thomas Liebscher, Andreas Niedeggen, Ulrich Dirnagl, Frank Bradke, Magdalena S Volz, Michael J DeVivo, Yuying Chen, Ulrich H von Andrian & Jan M Schwab in Nature Neuroscience. Published online September 18 2017 doi:10.1038/nn.4643

Abstract

Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex

Acute spinal cord injury (SCI) causes systemic immunosuppression and life-threatening infections, thought to result from noradrenergic overactivation and excess glucocorticoid release via hypothalamus–pituitary–adrenal axis stimulation. Instead of consecutive hypothalamus–pituitary–adrenal axis activation, we report that acute SCI in mice induced suppression of serum norepinephrine and concomitant increase in cortisol, despite suppressed adrenocorticotropic hormone, indicating primary (adrenal) hypercortisolism. This neurogenic effect was more pronounced after high-thoracic level (Th1) SCI disconnecting adrenal gland innervation, compared with low-thoracic level (Th9) SCI. Prophylactic adrenalectomy completely prevented SCI-induced glucocorticoid excess and lymphocyte depletion but did not prevent pneumonia. When adrenalectomized mice were transplanted with denervated adrenal glands to restore physiologic glucocorticoid levels, the animals were completely protected from pneumonia. These findings identify a maladaptive sympathetic-neuroendocrine adrenal reflex mediating immunosuppression after SCI, implying that therapeutic normalization of the glucocorticoid and catecholamine imbalance in SCI patients could be a strategy to prevent detrimental infections.

“Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex” by Harald Prüss, Andrea Tedeschi, Aude Thiriot, Lydia Lynch, Scott M Loughhead, Susanne Stutte, Irina B Mazo, Marcel A Kopp, Benedikt Brommer, Christian Blex, Laura-Christin Geurtz, Thomas Liebscher, Andreas Niedeggen, Ulrich Dirnagl, Frank Bradke, Magdalena S Volz, Michael J DeVivo, Yuying Chen, Ulrich H von Andrian & Jan M Schwab in Nature Neuroscience. Published online September 18 2017 doi:10.1038/nn.4643

Source: Springer.

Men and women with shorter, wider faces tend to be more sexually motivated and to have a stronger sex drive than those with faces of other dimensions. These are the findings from a study led by Steven Arnocky of Nipissing University in Canada. The research investigates the role that facial features play in sexual relationships and mate selection and is published in Springer’s journal Archives of Sexual Behavior.

The study adds to a growing body of research that has previously shown that certain psychological and behavioral traits are associated with particular facial width-to-height ratios (known as FWHR). Square-faced men (who therefore have a high FWHR) tend to be perceived as more aggressive, more dominant, more unethical, and more attractive as short-term sexual partners than their thinner and longer-faced counterparts.

Researchers attributed differences in facial proportions to variations in testosterone levels during particular developmental periods, such as puberty. This hormone plays a role in forming adult sexual attitudes and desires.

In this paper, Arnocky and his colleagues report two separate studies conducted among students. In the first, 145 undergraduates who were in romantic relationships at the time completed questionnaires about their interpersonal behavior and sex drive. The researchers also used photographs of the participants to determine their facial width-to-height ratio. The second study involved 314 students and was an extended version of the first study, which included questions about participants’ sexual orientation, the chances of them considering infidelity, and their sociosexual orientation. The latter is a measure of how comfortable participants are with the concept of casual sex that does not include love or commitment.

According to Arnocky, their findings suggest that FWHR can be used to predict a measure of sexuality in both sexes. Men and women with a high FWHR (therefore, square and wide faces) reported a greater sex drive than others.

“Together, these findings suggest that facial characteristics might convey important information about human sexual motivations” , says Arnocky.

It was also found that men with a larger FWHR not only have a higher sex drive than others, but also are more easy-going when it comes to casual sex and would consider being unfaithful to their partners.

Funding: Canadian Institutes of Health Research, Canada Research Chairs program funded this study.

Source: Stella Mueller – Springer
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will appear in Archives of Sexual Behavior.