Conclusion. – This study provides reference values for normal and pathological walking on treadmill and allows speed-dependent comparison between subjects. (C) 2008 Elsevier Masson SAS. All rights reserved.”
“Purpose: In elderly patients oxybutynin (Sigma-Aldrich (TM)) is commonly used to treat overactive bladder despite increased prevalence of Alzheimer’s disease in this population. We determined whether oxybutynin altered plaque formation, amyloid beta peptide expression and behavior in a transgenic mouse model of Alzheimer’s disease expressing the mutant human presenilin 1 (DeltaE9) and a chimeric mouse/human amyloid precursor protein (APPswe).

Materials and Methods: Mice were treated for 30 days in an acute experiment

or 5 months in a chronic experiment with oxybutynin (30 mg/kg) or vehicle. Behavioral testing was performed monthly with the elevated plus LB-100 maze (Med Associates, St. Albans, Vermont) in the chronic experiment. Brains were tested for plaque burden using Hirano silver and thioflavin-S (Sigma-Aldrich) staining. Amyloid beta peptide expression was tested using enzyme-linked immunosorbent assay for amyloid beta peptides 1-40 and 1-42.

Results: Animals treated with chronic oxybutynin had

a decreased plaque burden in the hippocampus (mean +/- SEM 2.2 +/- 0.4 vs 4.1 +/- 0.9 plaques, p <0.05) and cortex (5.8 +/- 0.7 vs 11.6 +/- 2.1, p <0.05) compared to animals treated with vehicle. Oxybutynin treated animals also had decreased expression of amyloid p 1-42 (82.8 +/- 9.0 eta learn more g/ml vs 105.6 +/- 5.5 eta g/ml, p = 0.05) compared to animals treated with Verteporfin vehicle. Female Alzheimer’s disease mice treated with oxybutynin but not males showed improved behavior with a greater percent of time spent in the closed arm or elevated plus maze (95.9% +/- 1.6% vs 35.6% +/- 18.9%, p <0.05). The greatest difference was noted at 3 months of treatment compared to vehicle.

Conclusions: These results suggest that oxybutynin may slow the progression of Alzheimer’s disease in this model.”
“Introduction. – Locomotion disorders are important in Huntington’s disease (HD). Although the rates of evolution of motor, functional or cognitive aspects

of HD have been studied, the evolution of locomotion disorders in early stages of the disease remains unknown.

Objectives. – To determine the rate of evolution of the HD-associated gait and gait initiation disorders and their correlates.

Patients and methods. – Eighteen HD patients were recorded with a minimum interevaluation interval of one year. Akinesia was studied by evaluating the anticipatory postural adjustment (APA) phase preceding the first step. We also evaluated gait speed, stride time and stride length.

Results. – We observed an alteration in the APA phase, whose evolution was correlated with that of akinesia. We also observed a decrease in gait speed, which was due both to an increase in stride time and a decrease in stride length.