Parkinson's disease (PD) is a progressive neurodegenerative disease. α-Synuclein (α-syn) oligomers play a critical role in the progression of PD. Baicalein, a typical flavonoid compound, can inhibit the formation of the α-syn oligomers, and disaggregate existing α-syn oligomers in vitro. However, whether baicalein could inhibit or disaggregate α-syn oligomers in vivo has not been investigated. Therefore, this study was designed to investigate the inhibitory effects of baicalein on α-syn oligomers in vivo and to explore the possible mechanisms of such inhibition. A chronic PD mouse model was created by continuous intragastric administration of rotenone (5mg/kg, 12weeks). Baicalein (100mg/kg) was intraperitoneally injected from 7week to 12week. Our result showed that the amount of α-syn, changes in the levels of the striatal neurotransmitters, and the behavioral changes found in the chronic PD mouse model were prevented after the baicalein injections. Although baicalein did not decrease α-syn mRNA expression, α-syn oligomers were significantly decreased in the ileum, thoracic spinal cord, and midbrain. Furthermore, transmission electron microscopy analysis showed that baicalein could prevent α-syn monomers from the oligomer formation in vitro. Taken together, these results suggest that baicalein could prevent the progression of α-syn accumulation in PD mouse model partly by inhibiting formation of the α-syn oligomers.

Neural stem cells (NSCs) can be isolated from nervous tissues or derived from embryonic stem cells. However, their procurement for clinical applications is limited, and there is a need for alternative types of cell that have NSCs properties. In the present study, the differentiation potential of rat adipose-derived stem cells (ADSCs) was evaluated by infecting these cells with a lentiviral vector-encoding green fluorescent protein (GFP). ADSCs transduced with lentivirus were able to generate NSC-like cells, without any effects on their growth, phenotype, and normal differentiation potential. NSC-like cells derived from ADSCs formed neurospheres and expressed high levels of the neural progenitor marker nestin. In the absence of selected growth factors, these neurospheres differentiated into neurons expressing NeuN and MAP2 and GFAP-expressing glia, as determined by immunocytochemistry, Western blotting, and quantitative real-time polymerase chain reaction. These results demonstrate that ADSCs can be induced to generate neurospheres that have NSC-like properties and may thus constitute a potential source of cells in stem cell therapy for neurological disorders.

Cerebral amyloid angiopathy (CAA) is a common degenerative disease presenting intracerebral hemorrhage (ICH) in older people. Uric acid (UA) is a natural antioxidant, and may have a beneficial role in neurodegenerative diseases. Nevertheless, the role of UA in CAA remains unknown. In the present study, we compared serum UA levels in CAA-associated ICH patients (n = 82) and age/sex-matched controls (n = 82). Serum UA levels in possible CAA were significantly decreased when compared with healthy controls (232.68 ± 77.70 vs. 309.42 ± 59.83 μmol/L; p < 0.001). Furthermore, UA levels in patients clinically diagnosed as probable CAA were significantly lower than those in patients diagnosed as possible CAA (193.06 ± 56.98 vs. 232.68 ± 77.70 μmol/L; p = 0.014). These differences were still significant after adjusting for renal function and dyslipidemia (p < 0.001 and p = 0.002, respectively). However, there were no associations between serum UA levels and the distribution of hemorrhagic lesion, as well as neurological impairment. Our observations indicate that serum UA levels were decreased in CAA patients. UA might play a neuroprotective role in CAA and serve as a potential biomarker for reflecting the severity of Aβ deposition.