Topic: alpha-synuclein

Protein quality control is essential for maintenance of a healthy and functional proteome that can attend the multiplicity of cellular functions. Failure of the systems that contribute to protein homeostasis, the so called proteostasis networks, have been identified in the pathogenesis of multiple neurodegenerative disorders and demonstrated to contribute to disease onset and progression. We are interested in autophagy, one of the components of the proteostasis network, and in the interplay of wo selective types of autophagy, chaperone-mediated autophagy (CMA) and endosomal microautophagy (eM

Parkinson's disease (PD), as the most prevalent neurodegenerative motor disorder, presents a complex spectrum of symptoms encompassing both motor impairments (bradykinesia, resting tremor, freezing of gait) and non-motor manifestations (depression, anosmia, anxiety). Robust animal models that faithfully replicate this multifaceted pathology are indispensable for comprehensive PD research. This study aims to investigate if depressive-like behaviour, prominent in up to 40% of PD patients (Laux, 2022), emerges in the bilateral human mutated alpha-synuclein (A53T) rat model of PD.40 adult Sprague-

Multiple System Atrophy (MSA) is a progressive neurodegenerative disorder due to the loss of various neuronal populations, including the GABAergic and the dopaminergic systems in the striatum and in the midbrain. The resulting degeneration of the nigro-striatal circuit is responsible for a severe neurological involvement characterized by parkinsonism and cerebellar phenotypes. The neuropathological hallmarks of MSA consist of alpha-synuclein aggregations in oligodendrocytes and neurons. No disease-modifying therapy is available for this disorder, resulting in a reduced life-span of affected pa

The striatum is densely innervated by midbrain dopamine (DA) neurons but also receives a further sparse monoaminergic innervation by raphe serotonin (5-HT) neurons. Striatal 5-HT has been suggested to have some opposing functions to DA but also to regulate DA release which might support (or counteract) this functional antagonism. We explored the reciprocal modulation of electrically evoked striatal DA and 5-HT release and the underlying cell circuits by using fast-scan cyclic voltammetry to detect DA, a new G-protein-coupled receptor sensor for 5-HT (GRAB5-HT3.0) and whole-cell recordings in a