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It is suggested that assessment of depressive symptoms may be clinically relevant in Parkinson's disease, particularly among patients with cognitive impairment.
This study suggests that polyG protein aggregates in NIID may shift the global RNA splicing profile toward an immature state, potentially through the sequestration of key splicing factors, such as SF3B4, thereby identifying new avenues for understanding the pathogenic mechanisms underlying NIID.
It is reported, in a large cohort, that GBA-mutated PD patients exhibit lower serum cholesterol levels and cholesterol supplementation was found to enhance the autophagic flux and mitigate α-synuclein accumulation in vitro, whereas AAV-Srebp2 delivery increased α-synuclein clearance in GbaL444P/+ mice.
The findings suggest the potential involvement of TMEM106B in the pathogenesis of disease progression in PD, especially in the deterioration of depression, cognition and QoL.
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