Publications by authors named "Mai Fujikura"
A 70-year-old woman presented with a 6-year history of cognitive dysfunction, neurogenic bladder, constipation and recurrent vomiting, and gradual worsening of symptoms. At the first admission to our department, she was also found to have hepatic encephalopathy due to intrahepatic portosystemic shunt. Head MRI revealed abnormal signal intensity at the corticomedullary junction, the splenium of the corpus callosum, and bilateral middle cerebellar peduncles on DWI.
View Article and Find Full Text PDFSIRT1 is involved in the regulation of a variety of biological processes such as metabolism, stress response, autophagy and differentiation. Although progenitor cells of oligodendrocytes (OPCs) express high level of SIRT1, its function on differentiation is unknown. Because we have shown that SIRT1 plays a pivotal role in differentiation of neural precursor cells, we hypothesized that SIRT1 may also participate in the differentiation of oligodendrocytes (OLGs).
View Article and Find Full Text PDFArticle Synopsis
- Microglia are crucial for clearing amyloid-β (Aβ) in Alzheimer's disease, and the study investigates how they take up Aβ through various receptors, specifically focusing on CD14 and Toll-like receptor 4 (TLR4).
- The research demonstrates that CD14 and TLR4 interact to internalize a specific type of Aβ, and that this process is influenced by clathrin-mediated endocytosis (CME).
- Findings indicate that both CD14 and TLR4 are not only involved in phagocytosis but also play a role in the clathrin-dependent uptake of Aβ, providing new insights that may inform potential Alzheimer's therapies.
Article Synopsis
- Alzheimer's disease (AD) is a leading cause of progressive dementia, primarily characterized by the accumulation of amyloid-β (Aβ) in the brain.
- Research indicates that reactive oxygen species (ROS) from mitochondria play a role in worsening AD, prompting a hypothesis about the early accumulation of Aβ and oxidative stress in brain mitochondria of a specific mouse model, APdE9.
- The study utilized electron paramagnetic resonance (EPR) and activity measurements of the antioxidant enzyme superoxide dismutase (SOD) to show that Aβ builds up in mitochondrial areas before non-mitochondrial areas, highlighting potential tools for understanding AD and developing treatments.
In response to changes of the central nervous system environment, microglia are capable of acquiring diverse phenotypes for cytotoxic or immune regulation and resolution of injury. Alzheimer's disease (AD) pathology also induces several microglial activations, resulting in production of pro-inflammatory cytokines and reactive oxygen species or clearance of amyloid-β (Aβ) through phagocytosis. We previously demonstrated that microglial activation and increase in oxidative stress started from the middle age in APPswe/PS1dE9 mice, and hypothesized that M1 activation occurs in middle-aged AD mice by Aβ stimulation.
View Article and Find Full Text PDFA 57-year-old man initially developed chest discomfort, nausea, vomiting, headache and low-grade fever, followed by paraplegia, sensory disturbance below level Th5 and bilateral visual loss. He was admitted to our hospital on the 15th day of illness. MRI short T1 inversion recovery image showed multiple longitudinal lesions in the spinal cord below C3, and T2-weighted image showed abnormal hyperintensity within the left optic nerve.
View Article and Find Full Text PDFAn 85-year-old woman was first admitted to our hospital because of right ptosis and diplopia. Examinations showed right oculomotor paralysis and reduced vision in the right eye. Serological and neuroradiological examinations failed to reveal the etiology.
View Article and Find Full Text PDF