Are there fetal stem cells in the maternal brain?

Fetal cells can enter maternal blood during pregnancy but whether they can also cross the blood-brain barrier to enter the maternal brain remains poorly understood. Previous results suggest that fetal cells are summoned to repair damage to the mother''s brain. If this is confirmed, it would open up new and safer avenues of treatment for brain damage caused by strokes and neural diseases. In this study, we aimed to investigate whether a baby''s stem cells can enter the maternal brain during pregnancy. Deceased patients who had at least one male offspring and no history of abortion and blood transfusion were included in this study. DNA was extracted from brain tissue samples of deceased women using standard phenol-chloroform extraction and ethanol precipitation methods. Genomic DNA was screened by quantitative fluorescent-polymerase chain reaction amplification together with short tandem repeat markers specific to the Y chromosome, and 13, 18, 21 and X. Any foreign DNA residues that could be used to interpret the presence of fetal stem cells in the maternal brain were monitored. Results indicated that fetal stem cells can not cross the blood-brain barrier to enter the maternal brain.     

Is zinc the link between compromises of brain perfusion (excitotoxicity) and Alzheimer's disease?

Prior brain injury is a major risk factor in the development of Alzheimer's disease. This is true for traumatic brain injury, stroke or ischemic brain injury, and (more speculatively) for brain injury resulting from the hypo-perfusion-reperfusion in cardiac arrest or cardiac bypass surgery and even hypo- or hypertension. Here we propose that the release of excess, toxic, "floods" of free zinc into the brain that occurs during and after all excitotoxic brain injury is a key factor that sets the stage for the later development of Alzheimer's disease. Rapid and aggressive administration of zinc buffering compounds to patients suffering brain injury may therefore not only ameliorate the acute injury but might also reduce the risk of subsequent development of Alzheimer's disease.     

Is monoamine oxidase inhibitor induced myoclonus serotoninergically mediated?

Summary In the present study a single case observation of myoclonus during sleep-wave transition was monitored in a depressed patient treated with the monoamine oxidase inhibitor, phenelzine. The myoclonus had a rhythm of 1 c/second and lasted for two years, the duration of phenelzine treatment. Myoclonus appeared neither during wakefulness nor during sleep, but at wake-sleep-wake transitions. This switch myoclonus was associated with phasic muscle hyperactivity during REM sleep.Methysergide a 5-HT suppressor, decreased the switch myoclonus frequency and the REM muscle hyperactivity, indicating serotoninergic involvement in the mechanism of phenelzine induced myoclonus.     

Why the maternal brain?

In the rat, the change from a virgin/nulliparous female to the maternal animal takes place at many levels. A subtle developmental wave washes over the female nervous system and transforms her from largely self-centred to offspring-directed, from personal care and protection to care of genetically-related offspring, from indifference to ardour. Such change is preceded by substantial and apparently permanent neural alterations, the depth of which results in the maternal brain, and is the basis of the present review. The neuroplasticity of pregnancy, inherent to the female brain and, we believe, representative of the full expression of the female nervous system's capacity, is a result of significant hormonal and other neurochemical actions. It results in the striking brain changes that are associated with, and necessary for, successful reproduction. We discuss some of these changes and their ramifications. Collectively, they represent the culmination of mammalian evolution and have led to the development of the social brain characteristic of higher orders of mammal, including the human. We also examine different facets of the maternal brain, beginning with a review of the genes involved in maternal behaviour, and in the subsequent 'expression' of the maternal brain. We next discuss olfaction and the manner in which this major sense draws from the rich sensory milieu of the mother to regulate and support maternal behaviour. Last, we discuss the 'whys' of maternal behaviour, a theoretical foray into the reasons for such substantial maternal brain alterations. We focus on the male's potential role as the raison d'etre for the manifest alterations in his mate's brain. In the end, it is clear that the female brain undergoes a significant reorganisation en route to motherhood, the results of which are deep and enduring.     

Is prosocial behaviour a missing link between green space quality and child health-related outcomes?

Social Psychiatry and Psychiatric Epidemiology - This study aimed to investigate prosocial behaviour—those behaviours that benefit others or enhance relationships with others—as a...     

What is the link between migraine and psychiatric disorders? From epidemiology to therapeutics

The association between migraine and psychiatric disorders is well documented through numerous population-based studies. The results of these studies are coherent and show an increased risk of suffering from depression, bipolar disorders, numerous anxiety disorders, especially post-traumatic stress disorder. This raises the question of stress as a precipitating factor for migraine illness. Psychiatric comorbidity is even more frequent in chronic migraine than in episodic migraine patients. Many prospective studies have shown that psychiatric comorbidity could be considered as a risk factor for migraine chronicization. Psychiatric comorbidity is also responsible for an increase of the frequency of anti-migraine drug intake, a worsening of quality of life and a worsening of functional impairment. It is also responsible for an increase in the direct and indirect costs of migraine. The reason why psychiatric comorbidity is so high in migraineurs is not unambiguous. Multiple causal relationships and common etiological factors are linked. Recently, genome-wide association studies gave leads to a genetic common heritability between major depressive disorder and migraine. For clinicians, an important topic remains how to treat migraineurs with psychiatric comorbidity. These patients suffer frequently from severe migraine or refractory migraine. Antidepressant and anti-convulsive drugs can be useful, as well as psychological therapies. But moreover, it is of utmost importance to propose an integrated multidisciplinary approach to these difficult patients.     

BDNF: a missing link between sympathetic dysfunction and inflammatory disease?

Nerve growth factor (NGF) plays a role in sympathetic neuron integrity and survival. Brain-derived neurotrophic factor (BDNF) also has trophic effects on sympathetic neurons. We report here the serendipitous finding that co-treatment of hippocampus with BDNF and the NGF antagonist TrkA-Fc leads to perivascular inflammation and marked vasoconstriction. This effect is not observed with either reagent alone or in combination with other control proteins. Because NGF supports sympathetic neuron health, we tested the hypothesis that BDNF combined with sympathetic compromise caused this effect. Superior cervical ganglia were removed bilaterally with concurrent BDNF infusion into hippocampus. Perivascular inflammation was observed at 3 days, but not 12 days post treatment, when sympathetic terminals had receded, suggesting that the presence of these terminals was necessary for inflammation. Since sympathetic dysfunction may lead to compensatory overactivity of norepinephrine (NE) signaling, we co-infused BDNF with NE in the hippocampus and observed perivascular inflammation. In humans, sympathetic overactivity has been reported in a variety of vascular diseases. Some of these diseases, e.g. primary Raynaud's, are not accompanied by serious inflammatory disease whereas others, such as scleroderma and systemic lupus, are. We speculate that BDNF may contribute to the transformation of sympathetic dysfunction to inflammatory disease.     

Is impulsivity a link between childhood abuse and suicide?

Childhood abuse and neglect are known to affect psychological states through behavioral, emotional, and cognitive pathways. They increase the risk of having psychiatric diseases in adulthood and have been considered risk factors for suicidal behavior in all diagnostic categories. Early, prolonged, and severe trauma is also known to increase impulsivity, diminishing the capacity of the brain to inhibit negative actions and to control and modulate emotions. Many neurobiological studies hold that childhood maltreatment may lead to a persistent failure of the inhibitory processes ruled mainly by the frontal cortex over a fear-motivated hyperresponsive limbic system. Multiple neurotransmitters and hormones are involved in the stress response, but, to our knowledge, the two major biological consequences of the chronic exposure to trauma are the hypofunction of the serotonergic system and changes in the hypothalamic-pituitary-adrenal axis function. Some of these findings overlap with the neurobiological features of impulsivity and of suicidal behavior. Impulsivity has also been said to be both a consequence of trauma and a risk factor for the development of a pathological response to trauma. Thus, we suggest that impulsivity could be one of the links between childhood trauma and suicidal behavior. Prevention of childhood abuse could significantly reduce suicidal behavior in adolescents and adults, in part, through a decrease in the frequency of impulsive behaviors in the future.     

Is there a link between adult neurogenesis and learning?

During the past several years, evidence has accumulated suggesting a relationship between newly born cells in the hippocampus and various types of learning and memory. However, most of the evidence is correlational and some of it does not agree. This review discusses both sides of this issue, considering the effects of learning on the production of new neurons in the dentate gyrus and the question of whether newly born cells participate in learning and memory.     

Is phentermine an inhibitor of monoamine oxidase? A critical appraisal

Phentermine produces a spectrum of concentration-dependent biochemical effects. It interacts with NE transporters at 0.1 microM, DA transporters at about 1 microM, 5-HT transporters at 15 microM and MAO-A at about 100 microM. When administered at typical anorectic doses, phentermine primarily interacts with DA and NE transporters and does not produce biochemical or neurochemical effects which would occur if it were inhibiting MAO-A. Some other explanation other than MAO inhibition must be sought to explain how oral phentermine increases platelet 5-HT, since platelet MAO-B does not metabolize platelet 5-HT, and since amphetamine-type drugs are even weaker inhibitors of MAO-B than MAO-A. Clinical studies in humans have shown that amphetamine, which is a more potent inhibitor of MAO-A than phentermine, does not inhibit MAO-A at therapeutic doses. Neither phentermine alone, fluoxetine alone or their combined use have been associated with cardiac valvulopathy, and clinical experience has shown their combined use to be free of significant adverse effects. Viewed collectively, there appears to be no data to support the hypothesis that phentermine inhibits MAO at typical therapeutic doses.     

On the link between attention deficit/hyperactivity disorder and obesity: do comorbid oppositional defiant and conduct disorder matter?

The link between attention deficit/hyperactivity disorder (ADHD) and elevated body weight/obesity can be regarded as well established. Because oppositional defiant disorder (ODD)/conduct disorder (CD) has also been found to be associated with these characteristics and ADHD and ODD/CD often occur comorbidly, we investigated whether ODD/CD and ADHD are independently linked with body weight and obesity. The clinical records of 360 children, 257 (6–12 years) with diagnoses of ADHD, ODD/CD, or comorbid ADHD and ODD/CD and 103 children with adjustment disorder (as a control group) constituted the database. All children were seen for the first time in two outpatient psychiatric clinics. Associations of the psychiatric diagnoses (ADHD present vs. not present; ODD/CD present vs. not present) with the standard deviation scores (according to German reference data) of the child’s body mass index (BMI-SDS) and presence of obesity were analyzed by ANCOVA and hierarchical logistic regression analysis, respectively. Children with ODD/CD showed higher BMI-SDS (F = 7.67, p < 0.006) and rate of obesity (Wald = 4.12, p < 0.05, OR = 2.43) while controlling for ADHD comorbidity. While adjusting for ODD/CD comorbidity, the links between ADHD and BMI-SDS or obesity did not reach statistical significance. Given a cross validation of these findings, future (preferably prospective longitudinal) research should analyze the mediating mechanism between the psychiatric conditions and obesity. This knowledge could be helpful for preventive interventions.