Depression frequently accompanies Parkinson's disease and often precedes the onset of motor symptoms. This study aimed to evaluate the impact of depression on motor compensation in patients with de novo Parkinson's disease. This retrospective cohort study analyzed data from 474 non-demented patients with de novo Parkinson's disease (mean age, 64.6±9.8 years; 242 men) who underwent both dopamine transporter PET scan and depression assessment using the Beck Depression Inventory at baseline. Patients were classified into tertiles by Beck Depression Inventory score. At baseline, high-tertile group (Beck Depression Inventory score ≥15, n = 157) showed more severe motor deficits and lower cognitive function than low-tertile group (Beck Depression Inventory score ≤7, n = 158, P = 0.034 and P = 0.008, respectively). Greater motor deficits in high-tertile group than low-tertile group remained significant after controlling for dopamine transporter binding in the posterior putamen, as well as other confounding variables. During follow-up of a median duration of 47 months, high-tertile group received higher levodopa-equivalent doses for symptom control than did low-tertile group after controlling for age, gender, and initial motor deficit severity. These results demonstrate that depression in de novo Parkinson's disease is associated with motor deficit severity at baseline and dose of PD medications during follow-up, suggesting that the presence of depression in de novo Parkinson's disease represents poor motor compensation.

Negative symptoms in schizophrenia can be categorized in the symptom-dimensions of apathy (avolition, anhedonia and social withdrawal) and reduced expression (blunted affect and alogia). Based on the strong relevance for the quality of life and functional outcome during the course of an illness, a differentiated diagnostic and therapeutic approach is of high importance. Such a differentiation specifies primary negative symptoms (regarded as an integral part of schizophrenia) and secondary negative symptoms (regarded as a result of positive symptoms, comorbid depression, effects of antipsychotic medication, substance abuse or social deprivation). The following overview will summarize the various aspects of negative symptoms and discuss current diagnostic and therapeutic recommendations.

Mitochondria are not just the powerhouses of the cell; these 'end of function' organelles are crucial components of cellular physiology and influence many central metabolic and signaling pathways that support complex multicellular life. Not surprisingly, these organelles play vital roles in adaptations for extreme survival strategies including hibernation and freeze tolerance, both of which are united by requirements for a strong reduction and reprioritization of metabolic processes. To facilitate metabolic rate depression, adaptations of all aspects of mitochondrial function are required, including; energetics, physiology, abundance, gene regulation, and enzymatic controls. This review discusses these factors with a focus on the stress-specific nature of mitochondrial genes and transcriptional regulators, and processes including apoptosis and chaperone protein responses. We also analyze the regulation of glutamate dehydrogenase and pyruvate dehydrogenase, central mitochondrial enzymes involved in coordinating the shifts in metabolic fuel use associated with extreme survival strategies. Finally, an emphasis is given to the novel mitochondrial research areas of microRNAs, peptides, epigenetics, and gaseous mediators and their potential roles in facilitating hypometabolism. © 2018 IUBMB Life, 2018.

Transdiagnostic cognitive behavioral interventions target different cognitive processes to promote mental health, including cognitive fusion and cognitive reappraisal. Determining the relative impact of cognitive fusion and reappraisal on a range of student mental health concerns could help interventions target psychopathological cognitive processes more effectively. Therefore, this study examined the longitudinal impact of cognitive fusion and reappraisal on mental health and functioning outcomes. A series of hierarchical regression models tested the effects of cognitive fusion and reappraisal in a sample of college students (n = 339). When controlling for reappraisal and baseline symptoms, fusion predicted distress, depression, generalized anxiety, social anxiety, hostility, academic distress, and student role problems 1 month later. Reappraisal predicted only student role problems longitudinally when controlling for fusion. These results suggest that cognitive fusion is a stronger predictor than reappraisal for a range of student mental health concerns and may be a particularly important target for improving student mental health.