Treadmill exercise represses neuronal cell death and inflammation during Aβ-induced ER stress by regulating unfolded protein response in aged presenilin 2 mutant mice.

Alzheimer's disease (AD) is characterized by the deposition of aggregated amyloid-beta (Aβ), which triggers a cellular stress response called the unfolded protein response (UPR). The UPR signaling pathway is a cellular defense system for dealing with the accumulation of misfolded proteins but switches to apoptosis when endoplasmic reticulum (ER) stress is prolonged. ER stress is involved in neurodegenerative diseases including AD, but the molecular mechanisms of neuronal apoptosis and inflammation by Aβ-induced ER stress to exercise training are not fully understood.

A quantitative electroencephalographic correlate of sustained attention processing.

The objective of the present investigation was to develop a quantitative electroencephalographic measure (qEEG) that is sensitive and specific to changes in sustained human performance. A principal components analysis (PCA) was performed on the qEEG obtained from participants during a continuous performance test. Measures of sensitivity (proportion of correctly identified correct responses, or hits) and specificity (proportion of correctly identified incorrect responses, or misses) were calculated to assess the classification accuracy of each newly derived component.