Background: It has been suggested that the protein Brain-derived Neurotrophic Factor (BDNF) plays a neuroprotective role in people with multiple sclerosis (pwMS). Also, BDNF seems to play a role in cognition performance. In the same line, gait in pwMS requires a higher cognitive resource, mainly during complex walking. Thus, maybe BDNF could be related to gait in pwMS.
Objective: To investigate the relationship between BDNF and gait spatial-temporal parameters during unobstructed and obstructed conditions and the Timed Up and Go (TUG) in pwMS and healthy controls (HC).
Methods: The study included 20 pwMS (11F/9M, 33.1±7.5 years, Expanded Disability Status Scale- EDSS 2.2±1.2) and 18 HC (13F/5M, 35.5±5.9 years). Both groups performed 20 gait attempts in two conditions: unobstructed walking (10 trials) and avoiding an obstacle. The obstacle was 15 cm in height and made of foam material. The BDNF serum concentration was collected with participants in fasting and completed before the clinical, gait, and mobility assessments. Clinical variables included the Symbol Digit Modality Test (SDMT), the Fatigue Severity Scale (FSS), and the International Physical Activity Questionnaire (IPAQ- short version). Associations between BDNF and spatial-temporal gait parameters, clinical variables, and TUG were determined by Pearson/Spearman correlations with Bonferroni's correction being applied (p<0.0013). Gait was compared by a two-way, repeated-measures ANOVA (group and condition) to characterize our cohort.
Results: Reduced BDNF was observed for pwMS (41.66±4.45 ng/ml) in comparison with HC (61.67±7.07, p<0.001). However, although some correlations presented a moderate correlation between BDNF with gait variables, the correlations didn't reach a significant p-value after Bonferroni's correction. Lastly, pwMS presented shorter step length and slower step velocity for both gait conditions, with more evidence for obstacle conditions. Only pwMS changed gait behavior from unobstructed walking to obstacle avoidance conditions (i.e., reduced step length and velocity and increased step duration).
Conclusion: BDNF is not related to either clinical (i.e., EDSS, SDMT, FSS, or IPAQ) or gait parameters in pwMS and HC, even in a condition involving higher cognitive demand. These results may suggest that BDNF does not play a role in these parameters' performance.
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http://dx.doi.org/10.1016/j.msard.2022.104064 | DOI Listing |
Mult Scler Relat Disord
October 2022
São Paulo State University (Unesp), School of Sciences, Graduate Program in Movement Sciences, Department of Physical Education, Human Movement Research Laboratory (MOVI-LAB), Bauru, SP, Brazil.
Background: It has been suggested that the protein Brain-derived Neurotrophic Factor (BDNF) plays a neuroprotective role in people with multiple sclerosis (pwMS). Also, BDNF seems to play a role in cognition performance. In the same line, gait in pwMS requires a higher cognitive resource, mainly during complex walking.
View Article and Find Full Text PDFMol Neurobiol
October 2021
Department of Pharmacology and Therapeutics, State University of Maringá, Av. Colombo, Maringá, Paraná, 5790, 87020-900, Brazil.
Evidence for the clinical use of neuroprotective drugs for the treatment of cerebral ischemia (CI) is still greatly limited. Spatial/temporal disorientation and cognitive dysfunction are among the most prominent long-term sequelae of CI. Cannabidiol (CBD) is a non-psychotomimetic constituent of Cannabis sativa that exerts neuroprotective effects against experimental CI.
View Article and Find Full Text PDFJ Neurosci
November 2008
Department of Biomedicine and Bergen Mental Health Research Center, University of Bergen, 5009 Bergen, Norway.
In a manner unique among activity-regulated immediate early genes (IEGs), mRNA encoded by Arc (also known as Arg3.1) undergoes rapid transport to dendrites and local synaptic translation. Despite this intrinsic appeal, relatively little is known about the neuronal and behavioral functions of Arc or its molecular mechanisms of action.
View Article and Find Full Text PDFJ Neurosci
August 2001
Program in Neuroscience, Department of Physiology and Howard Hughes Medical Institute, University of California, San Francisco, California 94143-0724, USA.
Previous work suggested qualitatively different effects of neurotrophin 3 (NT-3) in cochlear innervation patterning in different null mutants. We now show that all NT-3 null mutants have a similar phenotype and lose all neurons in the basal turn of the cochlea. To understand these longitudinal deficits in neurotrophin mutants, we have compared the development of the deficit in the NT-3 mutant to the spatial-temporal expression patterns of brain-derived neurotrophic factor (BDNF) and NT-3, using lacZ reporters in each gene and with expression of the specific neurotrophin receptors, trkB and trkC.
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