Article

Background In a combined animal and human study, we have previously found that a
5-day treatment that enhances cortical plasticity also facilitates brain-derived
neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling and
increases activated TrkB and N-methyl-d-aspartate receptor (NMDAR) association in
both the cortex and the peripheral lymphocytes.
Patients with Parkinson's disease
(PD), in general, show decreased cortical plasticity,
as demonstrated by
electrophysiological and behavioral studies. Here, we test the hypothesis that an
exercise program that improves motor function and seems to slow down symptom
progression can enhance BDNF-TrkB signaling in lymphocytes. Methods A total of 16
patients with PD underwent a 4-week multidisciplinary intensive rehabilitation
treatment (MIRT), which included aerobic training and physical and occupational
therapy. Blood was collected before and after 2 and 4 weeks of MIRT. Lymphocytes
were isolated to examine BDNF-TrkB signaling induced by incubation with
recombinant human BDNF. TrkB signaling complexes, extracellular-signal-regulated
kinase-2 and protein-kinase-B were immunoprecipitated; the content of
immunocomplexes was determined by Western blotting. Results After MIRT, all
patients showed improvement in motor function. TrkB interaction with NMDAR and
BDNF-TrkB signaling increased in peripheral lymphocytes at receptor,
intracellular mediator, and downstream levels. The decrements in Unified
Parkinson's Disease Rating Scale II (UPDRSII) and total scores were significantly
correlated with the increases in TrkB signaling at receptor, intracellular
mediator, and NMDAR interaction levels. Conclusions : The significant correlation
between reduced UPDRS scores and the changes in lymphocyte activity suggest that
enhanced BDNF-TrkB signaling in lymphocyte and reduced severity of PD symptoms
may be related.
CI - (c) The Author(s) 2015.

Langue : ANGLAIS