Associação entre a concentração sérica de fator neurotrófico derivado do cérebro (BDNF) e manifestações motoras e não motoras em indivíduos com doença de Parkinson

Abstract

Motor signs of Parkinson's disease (PD) result mainly from the degeneration of the dopaminergic neurons of the substantia nigra of the midbrain, which determines the dysfunction of the basal ganglia and affects the motor programming. In addition, other neurotransmitter systems are affected, such as serotonergic and noradrenergic, which explains the onset of nonmotor symptoms. The biological importance of brain-derived neurotrophic factor (BDNF) is well described in the literature, including the maintenance of neuroanatomic structures involved in motor behavior, as well as the relationship with other neurotransmitter systems. The present study had two objectives: 1. To evaluate if there is a difference in serum concentrations of BDNF and clinical measures and functional capacity between healthy individuals and PD; 2. Evaluate if there is an association between these concentrations, clinical measures and functional capacity in healthy individuals with PD. Evaluations of cognitive function, depression, fatigue and functional capacity (exercise capacity, walking speed and reaction time) were performed in both groups. In addition, individuals of the DP group were evaluated for severity of signs and symptoms of the disease, presence and severity of fatigue. The biological material was collected to measure the peripheral concentration of BDNF, using the ELISA method. Forty-seven patients, mean age of 67.4 years, enrolled in the mild to moderate stage in the disease, participated in the study. We evaluated 39 individuals from the control group, with a mean age of 65.5 years. Patients presented lower scores in the evaluation of cognitive function (p <0.001) and functional capacity tests (p <0.001) and higher scores in the evaluation of depression (p = 0.001). BDNF concentrations were lower in the DP group (p = 0.007). Statistically significant associations were found between these concentrations and the results obtained from functional capacity tests only in the control group. For the PD group, lower concentrations of BDNF were associated with higher depression scores and severity of symptoms in section I of the Unified Parkinson's Disease Scale. It is suggested that with the dopaminergic deficit and motor circuit dysfunction, the concentration of BDNF does not influence the functional performance in patients with PD. It should be noted that with inactivity, peripheral alterations of the musculoskeletal system are important factors that cause functional limitation, in addition to the progression of the disease itself. In contrast, non-motor changes of the disease (depression and behavioral changes, such as motivation) are associated with the concentration of BDNF, which corroborates other findings in the literature. Our results reaffirm the importance of knowing about BDNF alterations in individuals with PD and should be considered as potential for the therapeutic approach in these patients