Publications by authors named "K Kakuda"
Background: Paper symptom diaries are a common tool for assessing motor fluctuations in Parkinson's disease (PD) patients, but there are concerns about inaccuracies in the assessment of motor fluctuation due to recall bias and poor compliance. We, therefore, developed an electronic diary with reminder and real-time recording functions.
Objectives And Methods: To evaluate the effectiveness of the electronic diary, we compared compliance and motor fluctuation assessment with a paper diary.
The study aims to investigate the vitamin B6 levels in Parkinson's disease (PD) patients and their association with liver enzymes and evaluate how much dysregulation is associated with levodopa dose. Furthermore, to evaluate the effect of Opicapone, a catechol-o-methyl-transferase inhibitor, on vitamin B6 levels by monitoring the AST and ALT levels in patients treated with Levodopa-Carbidopa Intestinal Gel Infusion (LCIG). For these aims, serum vitamin B6 levels were measured (PD, n = 72 and controls, n = 31).
View Article and Find Full Text PDFLysophagy protects against propagation of α-synuclein aggregation through ruptured lysosomal vesicles.
Proc Natl Acad Sci U S A
January 2024
Article Synopsis
- The study investigates how misfolded α-synuclein (αSyn) spreads between neurons and contributes to diseases called synucleinopathies, focusing on the role of lysosomes.
- Researchers found that when αSyn aggregates invade lysosomes, they can cause the lysosomal membrane to rupture, leading to the transmission of αSyn aggregation to other neurons.
- The process of lysophagy, which is the selective degradation of damaged lysosomes, can prevent this transmission, suggesting that maintaining healthy lysosomes is crucial in managing the progression of synucleinopathies.
Lipid interaction with α-synuclein (αSyn) has been long implicated in the pathogenesis of Parkinson's disease (PD). However, it has not been fully determined which lipids are involved in the initiation of αSyn aggregation in PD. Here exploiting genetic understanding associating the loss-of-function mutation in Synaptojanin 1 (SYNJ1), a phosphoinositide phosphatase, with familial PD and analysis of postmortem PD brains, we identified a novel lipid molecule involved in the toxic conversion of αSyn and its relation to PD.
View Article and Find Full Text PDFArticle Synopsis
- Autophagy is a crucial cellular process that breaks down cytoplasmic materials to maintain balance within cells, involving the formation of autophagosomes that fuse with lysosomes to degrade contents.* -
- The study identified PACSIN1 as a vital regulator of autophagy, where its deletion reduced autophagic activity in normal nutrient conditions and caused buildup of amphisomes, suggesting it plays a role in lysosome fusion.* -
- PACSIN1 interacts with key proteins involved in autophagy and is shown to affect specific types of cargo degradation, indicating its importance in regulating differing pathways of autophagic processes depending on nutrient availability and stress.*