Marija Cvetanović

A neural basis for mutant ATAXIN-1 induced respiratory dysfunction in mouse models of Spinocerebellar ataxia type 1

This study identifies mutant ATAXIN-1's role in respiratory dysfunction in SCA1 mice by analyzing neural and skeletal muscle lineages.

Mutant ATXN1 impacts human and mouse microglia and contributes to cognitive, mood, and motor deficits in SCA1 mice

This study shows that mutant ATXN1 affects microglia in human and mouse models, leading to cognitive, mood, and motor deficits in SCA1 mice, which are ameliorated by reducing mutant ATXN1 in microglia.

Cerebellar contribution to cognitive deficits and prefrontal cortex dysfunction in Spinocerebellar Ataxia Type 1 (SCA1)

This study investigates how cerebellar dysfunction in SCA1 affects prefrontal cortex function and cognition, finding that cerebellar degeneration can both impair and ameliorate PFC dysfunction depending on disease context.

Altered calcium signaling in Bergmann glia contributes to Spinocerebellar ataxia type-1

This study shows that altered calcium signaling in Bergmann glia contributes to the electrophysiological changes in Purkinje cells in SCA1 mice, suggesting a therapeutic target for treatment.

Delineating regional vulnerability in the neurodegenerative disease SCA1 using a conditional mutant ATXN1 mouse

This study identifies brain regions and cell types contributing to SCA1 disease using conditional knockout mice, showing that targeting multiple areas and muscle is necessary for effective therapy.

Spatial and temporal diversity of astrocyte phenotypes in Spinocerebellar ataxia type 1 mice

This study examines spatiotemporal changes in astrocyte phenotypes in SCA1 mice, finding region-specific alterations in astrocyte function and homeostasis that may contribute to disease progression.

CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington's disease

This study shows that reducing CK2 in HD mice improves neuroinflammation, HTT aggregation, and motor deficits by reducing synucleinopathy.

Increased vulnerability of Purkinje cells in the posterior cerebellum of SCA1 mice is associated with molecular and cellular alterations related to disease pathology

The paper identifies regional transcriptional and physiological differences in Purkinje cells of the cerebellum in SCA1 mice, showing reduced heterogeneity and increased vulnerability in the posterior cerebellum.

Disrupting ATXN1 Nuclear Localization in a Knock-in SCA1 Mouse Model Improves a Spectrum of SCA1-Like Phenotypes and their Brain Region Associated Transcriptomic Profiles

This study shows disrupting ATXN1 nuclear localization in a SCA1 mouse model reduces disease-like phenotypes and alters region-specific transcriptomic profiles.

Single-nuclei RNA sequencing uncovers non-cell autonomous changes in cerebellar astrocytes and oligodendrocytes that may contribute to Spinocerebellar Ataxia Type 1 (SCA1) pathogenesis

The paper uses single-nuclei RNA sequencing to study glial cell changes in a SCA1 mouse model, identifying non-cell autonomous gene expression alterations in astrocytes and oligodendrocytes that may contribute to disease pathogenesis.