Impact of SAfinamide on Depressive Symptoms in Parkinson's Disease Patients (SADness-PD Study): A Multicenter Retrospective Study.

BACKGROUND: We aimed to assess the effects of safinamide on depression, motor symptoms, and the serotonin syndrome related to its co-administration with antidepressants in patients with Parkinson's disease (PD). METHODS: We retrospectively analyzed the data of patients at 1 and 3 months of follow-up compared to baseline. RESULTS: n = 82 (safinamide 50 mg = 22, 100 mg = 60, with antidepressants = 44). First, we found improvement in depression (Hamilton Depression Rating Scale: -6 ± 5.10 at 1 month and -7.27 ± 5.10 at 3 months, p < 0.0001; Patient Global Impression of Improvement Scale: 60.3% and 69.5% of patients at 1 and 3 months reported some improvement). Second, safinamide improved the daily life activities and motor symptoms/motor complications (Unified Parkinson's Disease Rating Scale (UPDRS-II): -2.51 ± 6.30 and -2.47 ± 6.11 at 1 and 3 months, p < 0.0001; III: -3.58 ± 8.68 and -4.03 ± 8.95 at 1 and 3 months, p < 0.0001; IV: -0.61 ± 2.61 and -0.8 ± 2.53 at 1 and 3 months, p < 0.0001). Third, 7.31% and 8.53% of patients developed non-severe adverse events related to safinamide at 1 and 3 months. Serotonin syndrome was not observed in the patients treated with antidepressants; some isolated serotonin syndrome symptoms were reported. CONCLUSIONS: Safinamide could be useful for treating depression in PD; it was effective for motor symptoms and motor complications and safe even when co-administered with antidepressants.

Early dysfunction of functional connectivity in healthy elderly with subjective memory complaints.

It is still an open question whether subjective memory complaints (SMC) can actually be considered to be clinically relevant predictors for the development of an objective memory impairment and even dementia. There is growing evidence that suggests that SMC are associated with an increased risk of dementia and with the presence of biological correlates of early Alzheimer's disease. In this paper, in order to shed some light on this issue, we try to discern whether subjects with SMC showed a different profile of functional connectivity compared with subjects with mild cognitive impairment (MCI) and healthy elderly subjects. In the present study, we compare the degree of synchronization of brain signals recorded with magnetoencephalography between three groups of subjects (56 in total): 19 with MCI, 12 with SMC and 25 healthy controls during a memory task. Synchronization likelihood, an index based on the theory of nonlinear dynamical systems, was used to measure functional connectivity. Briefly, results show that subjects with SMC have a very similar pattern of connectivity to control group, but on average, they present a lower synchronization value. These results could indicate that SMC are representing an initial stage with a hypo-synchronization (in comparison with the control group) where the brain system is still not compensating for the failing memory networks, but behaving as controls when compared with the MCI subjects.

Increased biomagnetic activity in healthy elderly with subjective memory complaints.

OBJECTIVE: Subjective memory complaints (SMCs) are frequently reported by elderly people with or without objective cognitive impairment (OMI) as assessed by neuropsychological tests. We investigate whether SMCs are associated with altered brain biomagnetic patterns even in the absence of OMI. METHODS: We report spatio-temporal patterns of brain magnetic activity recorded with magnetoencephalography during a memory task in 51 elderly participants divided into the following groups: patients with mild cognitive impairment (MCI) with SMC and OMI, individuals with SMC but not OMI, and healthy controls without neither SMC nor OMI. Exclusion criteria for all three groups included a diagnosis of depression or any other psychiatric condition. RESULTS: No statistically significant differences were found between MCI patients and participants with SMC. However, the SMC showed higher activation, between 200 and 900 ms after stimulus onset, than the control group in posterior ventral regions and in the dorsal pathway. MCI patients showed higher activation than the control group in the posterior part of the ventral pathway. CONCLUSIONS: These findings suggest that similar physiological mechanisms may underlie SMC and MCI, which could be two stages in a cognitive continuum. SIGNIFICANCE: MEG provide different neurophysiological profiles between SMC and control subjects.