Mental imagery and colour cues can prevent interference between motor tasks.

Motor interference can be observed when two motor tasks are learnt in subsequent order. The aim of the current study was to test two approaches potentially mitigating interference effects. The first approach used contextual colour cues requiring only little cognitive attention thus being assumed to be primarily implicit while the second, mental practice/rehearsal that demands much more active cognitive processing being considered explicit. Six groups performed a ballistic strength training immediately followed by the practice of an interfering visuomotor tracking task. Two groups received a contextual colour cue when presenting feedback about ballistic performance. During the practice of the interfering motor task, one of the two groups received the same colour cue during random trials while the other group received a different colour cue and a third control group no colour cue at all. The forth group mentally rehearsed the ballistic task during the practice of the interference task, while the respective control groups either mentally rehearsed a ramp and hold contraction instead of the ballistic task or didn't rehearse any task. The ballistic performance was tested before and after the ballistic training and in an immediate retention test after the learning of the interfering motor task. All groups significantly increased their ballistic performance after training. After practicing the interfering motor tracking, subjects receiving the same colour cue and subjects that mentally rehearsed the ballistic task did not show significant interference effect while all other groups did. These results indicate that implicit cuing with the same cue as well as explicit mental rehearsal of the initially learnt task can help to prevent motor interference without affecting performance improvements of the second motor task.

Cerebrospinal fluid BACE1 activity and brain amyloid load in Alzheimer's disease.

The secretase BACE1 is fundamentally involved in the development of cerebral amyloid pathology in Alzheimer's disease (AD). It has not been studied so far to what extent BACE1 activity in cerebrospinal fluid (CSF) mirrors in vivo amyloid load in AD. We explored associations between CSF BACE1 activity and fibrillar amyloid pathology as measured by carbon-11-labelled Pittsburgh Compound B positron emission tomography ([¹¹C]PIB PET). [¹¹C]PIB and CSF studies were performed in 31 patients with AD. Voxel-based linear regression analysis revealed significant associations between CSF BACE1 activity and [¹¹C]PIB tracer uptake in the bilateral parahippocampal region, the thalamus, and the pons. Our study provides evidence for a brain region-specific correlation between CSF BACE1 activity and in-vivo fibrillar amyloid pathology in AD. Associations were found in areas close to the brain ventricles, which may have important implications for the use of BACE1 in CSF as a marker for AD pathology and for antiamyloid treatment monitoring.

Amyloid clearance as a treatment target against Alzheimer's disease.

An imbalance between production and clearance of the amyloid-ß peptide (Aß) is a key momentum of the complex pathological cascade of Alzheimer's disease (AD). It is caused by overproduction of Aß or, more frequently, by impaired clearance from brain. Clearance can be reduced by increased aggregation, defective degradation, disturbed balance of transport across the blood-brain barrier, or inefficient peripheral removal of the peptide. In recent years these mechanisms have become targets of pharmacological interventions. Although several compounds have been discarded on the grounds of limited clinical efficacy, all major clearance-related approaches still hold promise. Some drug candidates have advanced to Phase III trials including anti-Aß antibodies, metal complexing agents, ginseng extracts, and intravenous immunoglobulins. Data are currently not available from these studies that might allow an evaluation of efficacy and safety. Phase II trials on active and passive immunization have demonstrated a striking discrepancy between significant neurobiological effects regarding the removal of Aß deposits and minor clinical outcomes. This does not preclude the possibility that clearance-related strategies have the potential of saving neurons and synapses via reducing the levels of soluble and particularly toxic Aß species in brain. It may take longer than projected in ongoing trials for such neurobiological effects to translate into measurable changes of clinical progression.