Signal peptide peptidase-like 2b modulates the amyloidogenic pathway and exhibits an Aβ-dependent expression in Alzheimer's disease.

Alzheimer's disease (AD) is a multifactorial disorder driven by abnormal amyloid β-peptide (Aβ) levels. In this study, we investigated the role of presenilin-like signal peptide peptidase-like 2b (SPPL2b) in AD pathophysiology and its potential as a druggable target within the Aβ cascade. Exogenous Aβ42 influenced SPPL2b expression in human cell lines and acute mouse brain slices.

Interactions of dopamine, iron, and alpha-synuclein linked to dopaminergic neuron vulnerability in Parkinson's disease and Neurodegeneration with Brain Iron Accumulation disorders.

Dopamine metabolism, alpha-synuclein pathology, and iron homeostasis have all been implicated as potential contributors to the unique vulnerability of substantia nigra dopaminergic neurons which preferentially decline in Parkinson's disease and some rare neurodegenerative disorders with shared pathological features. However, the mechanisms contributing to disease progression and resulting in dopaminergic neuron loss in the substantia nigra are still not completely understood. Increasing evidence demonstrates that disrupted dopamine, alpha-synuclein, and/or iron pathways, when combined with the unique morphological, physiological, and metabolic features of this neuron population, may culminate in weakened resilience to multiple stressors.

Cortical thickness, white matter hyperintensities, and cognition after stroke.

Background: A thinner cerebral cortex is associated with higher white matter hyperintensity burden and cognitive impairment in community-dwelling and dementia cohorts. It is important to assess these associations in people with ischemic stroke because their cerebrovascular disease profiles are different to these cohorts.

Aims: We aimed to determine whether cortical thickness was related to white matter hyperintensity burden and cognition after ischemic stroke.

The specificity of temporal expectancy: evidence from a variable foreperiod paradigm.

In speeded choice tasks with variable foreperiods (FPs), individuals behaviourally adapt to various frequency manipulations. Adaptations have been shown to frequencies of different stimulus-response events, to frequencies of different foreperiods, and to frequencies of different event-foreperiod combinations. We have investigated how participants adapt to a situation where all three frequency manipulations are done simultaneously.

The scope and precision of specific temporal expectancy: evidence from a variable foreperiod paradigm.

Recent evidence from choice response time experiments with variable foreperiods (FPs) has shown that temporal expectancy can be event specific. When a certain target appears particularly frequent after one certain FP, participants tend to expect that target after that FP. This typically results in best performance for that target when it appears after that FP.

Temporal cueing of target-identity and target-location.

In four experiments either a short or a long foreperiod preceded the presentation of one of two targets, presented either in the center of the screen (Experiment 1) or at one of two locations (Experiments 2-4). Participants were to identify the presented target by pressing a left or a right button as quickly as possible. In Experiment 1, each of the two targets and in Experiment 2, each of the two locations appeared frequently after one and infrequently after the other foreperiod.

Unconscious manipulation of free choice in humans.

Previous research has shown that subliminally presented stimuli accelerate or delay responses afforded by supraliminally presented stimuli. Our experiments extend these findings by showing that unconscious stimuli even affect free choices between responses. Thus, actions that are phenomenally experienced as freely chosen are influenced without the actor becoming aware of the manipulation.

Evidence for unaltered brain electrical topography during prefrontal response control in cycloid psychoses.

Objective: Prefrontal structures such as the anterior cingulate cortex (ACC) play a decisive role in processes of action monitoring and response control, functions often impaired in schizophrenia. Patients with cycloid psychoses exhibit some characteristic neurophysiological features not indicative of the cerebral hypofrontality observed in schizophrenia. This study aimed at examining if cycloid psychoses-unlike schizophrenias-involve a normal brain-electrical topography during a task demanding prefrontal response control.

Allelic variation of serotonin transporter function modulates the brain electrical response for error processing.

A functional length variation in the transcriptional control region of the serotonin transporter gene (5-HTTLPR) influences brain function, personality traits, and susceptibility to psychiatric disorders. Here we measured prefrontal brain function by means of event-related potentials during an error processing paradigm. Physiologically, occurrence of an error elicits two specific electrical responses in the prefrontal cortex, the early error related negativity (Ne/ERN) and the later occurring error positivity (Pe), reflecting different components of error processing.