The spatial and linguistic division of the city of Malaga

The city of Malaga underwent considerable growth in the 19th and 20th centuries. The territorial expansion paired with a massive influx of immigrants occurred in three waves and as a consequence the city of Malaga remains divided into three different parts up to today. The differences between these three neighbourhoods of the city lie in the type of houses, different cultural and industrial activities, socioeconomic level, and very interestingly, also in speech. Thus, the aim of this study is an examination of the interrelation between speech (phonetic features) and urban space in Malaga. A combination of quantitative and qualitative analysis was used, based on two types of data: 1) production data stemming from recordings of 120 speakers; 2) perception data (salience, estimated frequency of use, attitude, spatial and social perception, imitation) which was collected from several surveys with 120 participants each. Results show that the speech production data divides the city of Malaga clearly into three different parts. This tripartition is confirmed by the analysis of the perception data. Moreover, the habitants of these three areas are perceived as different social types, to whom a range of social features is attributed. That is, certain linguistic features, the different neighbourhoods of the city and the social characteristics associated with them are undergoing a process of indexicalization and iconization. As a result, the linguistic features in question function as identity markers on the intraurban level.

Mitochondrial impairments contribute to Spinocerebellar ataxia type 1 progression and can be ameliorated by the mitochondria-targeted antioxidant MitoQ

Spinocerebellar ataxia type 1 (SCA1), due to an unstable polyglutamine expansion within the ubiquitously expressed Ataxin-1 protein, leads to the premature degeneration of Purkinje cells (PCs), decreasing motor coordination and causing death within 10-15 years of diagnosis. Currently, there are no therapies available to slow down disease progression. As secondary cellular impairments contributing to SCA1 progression are poorly understood, here, we focused on identifying those processes by performing a PC specific proteome profiling of Sca1154Q/2Q mice at a symptomatic stage. Mass spectrometry analysis revealed prominent alterations in mitochondrial proteins. Immunohistochemical and serial block-face scanning electron microscopy analyses confirmed that PCs underwent age-dependent alterations in mitochondrial morphology. Moreover, colorimetric assays demonstrated impairment of the electron transport chain complexes (ETC) and decrease in ATPase activity. Subsequently, we examined whether the mitochondria-targeted antioxidant MitoQ could restore mitochondrial dysfunction and prevent SCA1-associated pathology in Sca1154Q/2Q mice. MitoQ treatment both presymptomatically and when symptoms were evident ameliorated mitochondrial morphology and restored the activities of the ETC complexes. Notably, MitoQ slowed down the appearance of SCA1-linked neuropathology such as lack of motor coordination as well as preventing oxidative stress-induced DNA / RNA damage and PC loss. Our work identifies a central role for mitochondria in PC degeneration in SCA1 and provides evidence for the supportive use of mitochondria-targeted therapeutics in slowing down disease progression.