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Neurorehabil Neural Repair. 2016 Jun;30(5):411-8. doi: 10.1177/1545968315600272. Epub 2015 Aug 7.

Intensive Rehabilitation Enhances Lymphocyte BDNF-TrkB Signaling in Patients With Parkinson's Disease.

Author information

1
Sophie Davis School for Biomedical Education at CCNY, CUNY, New York, NY, USA The Graduate Center, CUNY, New York, NY, USA.
2
Sophie Davis School for Biomedical Education at CCNY, CUNY, New York, NY, USA.
3
"Moriggia Pelascini" Hospital, Gravedona ed Uniti, Italy.
4
The Fresco Institute for Parkinson's & Movement Disorders, NYU-Langone School of Medicine, New York, NY, USA.
5
Istituti Clinici di Perfezionamento, Milano, Italy.
6
The Fresco Institute for Parkinson's & Movement Disorders, NYU-Langone School of Medicine, New York, NY, USA IRCCS Centro Neurolesi "Bonino-Pulejo", Messina, Department of Neuroscience, University of Messina, Italy.
7
Sophie Davis School for Biomedical Education at CCNY, CUNY, New York, NY, USA The Fresco Institute for Parkinson's & Movement Disorders, NYU-Langone School of Medicine, New York, NY, USA lice.mg79@gmail.com.

Abstract

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.

KEYWORDS:

LTP; human; immune system; plasticity

PMID:
26253177
PMCID:
PMC4744811
DOI:
10.1177/1545968315600272
[Indexed for MEDLINE]
Free PMC Article

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