No abstract

In Parkinson disease (PD), apathy and depression often overlap, making it difficult to differentiate between them. This study sought to analyze apathy and depression in patients with PD dementia (PDD). Forty patients were diagnosed with PDD using the Movement Disorder Society criteria. A statistically significant correlation was identified between worsening dementia and an improvement in depression ( r = .3695; r = .1365, 95% confidence interval [CI]: 0.0985 to 05.894, P = .0044) and between worsening dementia and worsening apathy ( r = -.2578, r = .0664, 95% CI: -0.5025 to .0251, P = .036). Depression had a greater correlation with advanced motor symptoms ( r = .4988, r = .2438, 95% CI: 0.2218-0.7013, P = .0005]. In conclusion, depression was associated with less advanced PDD and more intense motor features, while apathy was associated with more advanced cognitive impairment.

possibility of cancer, he was submitted to an upper gastrointestinal endoscopy, which suggested pangastritis. The gastric estrongiloidiasis diagnosis was further confirmed in the histopatologic analysis, which revealed the presence of S. stercoralis' eggs and worms. DISCUSSION: Even though the stomach involvement is rare, patients whose gastric mucosa is infected are more likely to evolve to the severe forms. Gastroduodenal ulcers and perforations have been reported as possible complications. Stool examination is considered the gold standard diagnostic method, but the histopatologic analysis may be valuable when stool examination fails. The treatment does not depend on the infection's site and ivermectin is the first line therapy.

No abstract

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.