Different motor tasks impact differently on cognitive performance of older persons during dual task tests

Background

Dual task paradigm states that the introduction of a second task during a cognitive or motor performance results in a decreased performance in either task. Treadmill walk, often used in clinical applications of dual task testing, has never been compared to overground walk, to ascertain its susceptibility to interference from a second task. We compared the effects of overground and treadmill gait on dual task performance.

Methods

Gait kinematic parameters and cognitive performance were obtained in 29 healthy older adults (mean age 75 years, 14 females) when they were walking freely on a sensorized carpet or during treadmill walking with an optoelectronic system, in single task or dual task conditions, using alternate repetition of letters as a cognitive verbal task.

Findings

During overground walking, speed, cadence, step length stride length, and double support time (all with P value < 0.001) and cognitive performance (number of correct words, P < 0.001) decreased substantially from single to dual task testing. When subjects walked at a fixed speed on the treadmill, cadence decreased significantly (P = 0.005), whereas cognitive performance remained unaffected.

Interpretation

Both motor and cognitive performances decline during dual task testing with overground walking. Conversely, cognitive performance remains unaffected in dual task testing on the treadmill. In the light of current dual task paradigm, these findings may have relevant implication for our understanding of motor control, as they suggest that treadmill walk does not involve brain areas susceptible to interference from the introduction of a cognitive task.     

Dual action of chronic ethanol treatment on LPS-induced response in C6 glioma cells

The importance of the classical immune molecule, class I major histocompatibility complex to central nervous system function is one of the most surprising discoveries related to neuroimmunology in the past decade. Mice lacking both β-2microglobulin and transporter associated with antigen processing (β2M-/-TAP-/-) showed differences in basal behavior. In response to saline injection, β2M-/-TAP-/- mice showed a significant hypothalamic pituitary adrenal activation that was not observed in wild type mice, while lipopolysaccharide-induced cytokine expression in the hypothalamus was similar in β2M-/-TAP-/- and wild type mice. Overall, these data show that class I MHC plays an important role in behavior and stress reactivity.     

Evidence that AKT and GSK-3β pathway are involved in acute hyperhomocysteinemia

Homocysteine is a neurotoxic amino acid that accumulates in several disorders including homocystinuria, neurodegenerative and neuroinflammatory diseases. In the present study we evaluated the effect of acute and chronic hyperhomocysteinemia on Akt, NF-κB/p65, GSK-3β, as well as Tau protein in hippocampus of rats. For acute treatment, rats received a single injection of homocysteine (0.6 μmol/g body weight) or saline (control). For chronic treatment, rats received daily subcutaneous injections of homocysteine (0.3-0.6 μmol/g body weight) or saline (control) from the 6th to the 28th days-of-age. One or 12h after the last injection, rats were euthanized, the hippocampus was removed and samples were submitted to electrophoresis followed by Western blotting. Results showed that acute hyperhomocysteinemia increases Akt phosphorylation, cytosolic and nuclear immunocontent of NF-κB/p65 subunit and Tau protein phosphorylation, but reduces GSK-3β phosphorylation at 1h after homocysteine injection. However, 12h after acute hyperhomocysteinemia there is no effect on Akt and GSK-3β phosphorylation. Furthermore, chronic hyperhomocysteinemia did not alter Akt and GSK-3β phosphorylation at 1h and 12h after the last administration of this amino acid. Our data showed that Akt, NF-κB/p65, GSK-3β and Tau protein are activated in hippocampus of rats subjected to acute hyperhomocysteinemia, suggesting that these signaling pathways may be, at least in part, important contributors to the neuroinflammation and/or brain dysfunction observed in some hyperhomocystinuric patients.