Nerve growth factor (NGF) is the prototype of related neurotrophic proteins, the so-called neurotrophins. NGF is essential for proper development of sympathetic and neural crest-derived sensory neurons of the peripheral nervous system (PNS) as well as of the neurons in the cholinergic basal forebrain (CBF). In the mature peripheral and central nervous system (CNS) NGF is also biologically active; NGF facilitates neuronal plasticity and regulates synaptic transmission and connectivity. Besides this well established neurotrophic function, recent findings suggest a role of NGF in neuroimmune and stress-associated processes, which NGF imparts not only as the classical "target-derived messenger", that is retrogradely transported within NGF-sensitive neurons, but also as para- and autocrine cytokine modulating the function of non-neuronal cells. Since neurotrophins are produced in very small amounts in vivo, NGF-sensitive cells have to compete for the limited NGF even under physiological conditions, so that normally only less than 10% of NGF receptors (NGFR) are saturated with their endogenous ligand. Consequently, it is feasable that minute changes in NGF concentrations can influence neuronal function in an extensive way. Hence, one plausible pathomechanism of disease(s) may be that a deficiency in NGF leads to malfunction of NGF-sensitive neurons. The change in NGF concentrations in the course of several diseases, namely during alcoholic and diabetic neuropathy as well as in Alzheimer's disease (AD) and several lesion-models of the CBF, indicates that fluctuations of endogenous NGF concentrations in PNS and CNS follow a distinctive pattern. An initial deficit of NGF at the onset of pathological processes is typically followed by its temporary elevation, during which some neuronal deficits may be partially ameliorated. However, if the disease progresses a decrease of NGF is typically observed, which appears to be a "normalization" of formerly elevated NGF concentrations. In our hypothesis we postulate that after acute or chronic injuries NGF is up-regulated as an intrinsic attempt to regenerate NGF-sensitive neurons. After long-term exposure to noxious processes, however, this compensatory increase of NGF cannot be maintained and eventually breaks down. The extent of such a compensatory up-regulation may depend on age and condition of NGF-sensitive neurons as well as on the type of lesion (acute or chronic). Furthermore, we also postulate that an exceeding level of NGF or its chronic elevation could even be detrimental to neuronal functioning under certain conditions. Thus, endogenous NGF has the capacity to modulate and even to compensate different kinds of harmful processes and in this way it may reinstate the homeostatic equilibrium. In our view, it seems to be a more appropriate approach to regard NGF changes as independent of classical constructs of neuropsychiatric diseases. Perhaps our understanding of NGF may even model for a new approach to the aetiology of multifactorial neuropsychiatric disorders.
Affective dysregulation is a core feature of borderline personality disorder, and some patients also report dissociative symptoms. The present study investigated the temporal relations between arousal and valence dimensions of affect and dissociative states using micro-assessments in daily life. Patients with borderline personality disorder (n = 42) or depressive disorders (n = 40), and non-clinical controls (n = 39) reported affective and dissociative states every 15 min for 13 hours (52 times). Dynamic structural equation modeling showed the highest levels of average daily arousal, negative affect, and dissociative states in patients with borderline personality disorder, as expected. In addition, increased arousal linearly predicted stronger dissociative states in the next measurement, especially for negative affective valence, in patients with borderline personality disorder. Finally, descriptive results indicated that negative affective valence decreased following increased dissociative states in patients with borderline personality disorder. These findings suggest that changes in affect play an important role at the onset of dissociations and may explain why dissociations are maintained. Clinicians should provide patients with adaptive means to regulate high levels of arousal when helping them to deal with dissociative symptoms.
Borderline personality disorder (BPD) is characterized by high levels of arousal and perceived rejection by others. The temporal relation between these constructs, however, remains largely unclear. Based on predictions derived from the dynamic affect model and the rejection sensitivity model, we expected increases in arousal and perceived rejection to predict subsequent increases in perceived rejection and arousal, respectively. To investigate this topic, we assessed current self-reported affective arousal and perceived rejection in patients with BPD (n = 42), patients with depressive disorders (DDs; n = 43), and healthy controls (HCs; n = 40) for 52 times within 13 hr (ca. every 15 min). In line with previous studies, dynamic structural equation model results indicate significantly higher trait levels of arousal and perceived rejection in patients with BPD compared with participants in the DD and HC groups. In addition, we found substantial autoregressive and cross-lagged effects for arousal and perceived rejection. Other than expected, the magnitude of these effects did not significantly differ across diagnostic groups. Our findings suggest close temporal relations between arousal and perceived rejection. In patients with BPD, these effects unfold against the background of substantially elevated trait levels of arousal and perceived rejection. Future experience sampling studies should provide additional context information (e.g., through monitoring rejection events) to investigate how patients with BPD perceive rejection in everyday life and how this affects subsequent levels of arousal.
Patients with borderline personality disorder (BPD) are getting significantly better under inpatient Dialectic Behavioral Therapy (DBT). Several studies have shown the efficacy of DBT inpatient treatment for patients with BPD. Signs of the efficacy of DBT are mainly reduction of self-injurious behaviour and suicidality as well as reduction of clinical parameters such as depression and general symptom stress (SCL-90-R). In this catamnestic study we evaluated 38 former DBT-inpatients for continuous treatment effects of DBT. The results showed a significant reduction in depression as well as general symptom stress up to 6 month after discharge. Furthermore, these effects were positively correlated with the continuous use of DBT-skills 1 and 6 months after discharge. These skills are central part of DBT-treatment and are especially useful for managing high-tension, suicidality and self-injurious behaviour. Therefore, the use of skills is possibly the reason for the continuous effect of DBT after the end of inpatient treatment.
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