BackgroundScreening tests have been used for cognitive deficits in Parkinson's disease (PD).ObjectiveThis study compared the Montreal Cognitive Assessment (MoCA) test, the Mini-Mental State Examination (MMSE) and the clock drawing test for this purpose.MethodsA total of 50 patients with PD were selected, 41 (82%) were diagnosed with dementia by the criteria of the Movement Disorder Society. The test Scales for Outcomes in Parkinson's Disease-Cognition (SCOPA-Cog) was used as the gold standard in comparison with the screening tests.ResultsThe MoCA test (AUC=0.906) had a sensitivity of 87.80% and specificity of 88.89%. When the MMSE was associated with the clock drawing test (AUC=0.936), it had a specificity of 66.67% and sensitivity of up to 97.56%.ConclusionThe study suggests that the MoCA test can be a good screening test in PD. However, MMSE associated with the clock drawing test may be more effective than the MoCA test.
Patients with Parkinson disease dementia (PDD) have deficits resulting mainly from frontostriatal dysfunction. The aim of this study was to assess the effectiveness of reality orientation therapy (ROT) combined with drug therapy (acetylcholinesterase inhibitors) in PDD treatment and compare it with that of drug therapy alone. Patients (n ¼ 12) with a diagnosis of PDD were divided into 2 groups: group A-drug therapy and ROT; group B-drug therapy alone. Reality orientation therapy was applied weekly for 6 months, and patients were assessed during the same period. Significant improvements in frontostriatal deficits were observed in the group that received the combined therapy, as shown mainly by the scores in verbal fluency in the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) battery (P ¼ .02) and in attention in Scales for outcomes of Parkinson's Disease-Cognition (P ¼ .021) and Clock Drawing Test (P ¼ .037). Patients who received only medication had worse results in constructional praxis recall in the CERAD battery (P ¼ .037). Our results indicate that ROT may help in the treatment of frontostriatal cognitive deficits and can potentially be used to complement drug therapy.
The literature on computerized models that help detect, study and understand signs of mental health disor- ders from social media has been thriving since the mid-2000s for English speakers. In Brazil, this area of research shows promising results, in addition to a variety of niches that still need exploring. Thus, we construct a large corpus from 2941 users (1486 depressive, 1455 non-depressive), and induce machine learning models to identify signs of depression from our Twitter corpus. In order to achieve our goal, we extract features by measuring linguistic style, behavioral patterns, and affect from users’ public tweets and metadata. Resulting models successfully distinguish between depressive and non-depressive classes with performance scores comparable to results in the literature. We hope that our findings can become stepping stones towards more methodologies being applied at the service of mental health.
Synuclein and tau drive pathogenesis, and tissues from AD and PD patients sometimes display accumulations of both proteins. Some studies have shown that these two proteins can seed each other's formation of toxic moieties, but it remains unclear what increases the levels of both proteins. To uncover common pathogenic pathways and identify molecules that might reduce toxicity in these two diseases, we screened for modifiers affecting the steadystate levels of both alpha-Synuclein and tau. We found that TRIM28 regulates both alpha-Synuclein and tau stability in human cells, Drosophila and mouse brain and that reduction of TRIM28 rescues toxicity in Drosophila and mouse models of alpha-Synuclein-and taumediated degeneration. We further discovered that TRIM28 promotes alpha-Synuclein and tau stability and toxicity through SUMOylation and subsequent nuclear translocation and that this accelerates pathology in mouse models of synucleinopathy and tauopathy. This study underscores the importance for intersecting screens across comorbid proteinopathies to reveal shared mechanisms.
Synuclein and tau drive pathogenesis, and tissues from AD and PD patients sometimes display accumulations of both proteins. Some studies have shown that these two proteins can seed each other's formation of toxic moieties, but it remains unclear what increases the levels of both proteins. To uncover common pathogenic pathways and identify molecules that might reduce toxicity in these two diseases, we screened for modifiers affecting the steadystate levels of both alpha-Synuclein and tau. We found that TRIM28 regulates both alpha-Synuclein and tau stability in human cells, Drosophila and mouse brain and that reduction of TRIM28 rescues toxicity in Drosophila and mouse models of alpha-Synuclein-and taumediated degeneration. We further discovered that TRIM28 promotes alpha-Synuclein and tau stability and toxicity through SUMOylation and subsequent nuclear translocation and that this accelerates pathology in mouse models of synucleinopathy and tauopathy. This study underscores the importance for intersecting screens across comorbid proteinopathies to reveal shared mechanisms.
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