Effects of night shifts in bipolar disorders and extreme morningness.

BACKGROUND: Night work and shift work scenarios are increasing in modern society. Instability in the sleep-wake rhythm is an important risk factor for triggering episodes of bipolar disorder. Extreme chronotype has negative effects on shift work ("shift-worker syndrome"). Effects of night or shift work on patients with bipolar disorder and extreme chronotype are not well understood. CASE REPORT: A patient with bipolar II disorder and extreme morning type followed a stable work schedule for a significant period of time, maintaining a stable mood. After changing to a night-shift schedule, depressive symptoms developed. When the night-shift schedule was stopped, her mental state normalised. CONCLUSIONS: This case highlights the possibility of a sensitizing role of chronotype in triggering episodes of bipolar disorder after the sleep-wake rhythm has been disrupted by night work or shift work. The evaluation of a person's capability to perform night work or shift work should take into account psychiatric disorders and chronotype as well as physical conditions.

Daytime impairment and neurodegeneration in OSAS.

STUDY OBJECTIVE: Controversy surrounds the pathogenesis of neurocognitive daytime dysfunction exhibited by patients with obstructive sleep apnea syndrome (OSAS). Underlying brain dysfunctions and damage have long been suspected as a cause of some of this impairment. Neuroimaging has enabled scientists to test these long-held theories. This paper is based on a comprehensive review of recent publications on neuroimaging studies in this area. It seeks to highlight results of recent research, which suggest connections between persistent neurocognitive daytime impairment of executive functions, underlying signs of cerebral metabolic impairment and neurodegeneration, considering possible cerebrovascular impairment in OSAS patients. We propose the existence of a neurodegenerative process.

Electrophoretic separation of amyloid beta peptides in plasma.

In this prospective study, for the first time we have separated and quantified amyloid beta (Abeta) peptides in the plasma of patients with Alzheimer's disease (AD, n = 8) and age- and environment-matched healthy controls (n = 9) with urea-based Abeta-sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE)/immunoblot. In addition to the Abeta peptides 1-37/38/39/40/42, which we recently identified as regular constituents of human cerebrospinal fluid (CSF), we have observed a novel electrophoretic band migrating slightly cathodically to Abeta1-42. Since a standard peptide with the amino acid sequence Abeta2-40 migrates in the same position, we hypothesize that this plasma-specific band may correspond to Abeta2-40. The concentration of Abeta peptides in the plasma has been approximately 100-fold lower compared to the CSF. Interestingly, the concentration of the two shortest peptides and the longest one of these considered here (i.e., Abeta1-37/38/42) have increased significantly when the samples have been frozen at -80 degrees C before immunoprecipitation, while the 'middle-length' peptides (i.e., Abeta1-39/40) have not been affected by this procedure. We have not observed significant differences of the Abeta peptides concentrations between AD and control subjects. Our method can be used to investigate the significance of plasma Abeta peptides in neurodegenerative disorders, and to monitor the efficiency of drugs with beta/gamma-secretase inhibitory potency.