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| http://dx.doi.org/10.1016/j.trci.2018.03.008 | DOI Listing |
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Electric-field induced sleep promotion and lifespan extension in Gaucher's disease model flies.
Biochem Biophys Rep
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Institute for Chronobiology, Foundation for Advancement of International Science (FAIS), 3-24-16 Kasuga, Tsukuba, Ibaraki, 305-0812, Japan.
Gaucher's disease (GD) is a genetic disease characterized by a mutation in the metabolic enzyme glucocerebrosidase (GBA1), leading to the accumulation of glucosylceramide in tissues. We previously discovered that a -inserted mutation in the gene of fruit flies, , mimics human neuronopathic GD (nGD) characteristics, providing a promising model for studying the molecular mechanisms of the disease. We also reported that extremely low-frequency electric fields (ELF-EFs) promote sleep and extend the lifespan of wild-type flies.
View Article and Find Full Text PDFUnderstanding retinal tau pathology through functional 2D and 3D iPSC-derived in vitro retinal models.
Acta Neuropathol Commun
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Department of Physiology and Pharmacology, Sapienza University of Rome, 00185, Rome, Italy.
The generation of retinal models from human induced pluripotent stem cells holds significant potential for advancing our understanding of retinal development, neurodegeneration, and the in vitro modeling of neurodegenerative disorders. The retina, as an accessible part of the central nervous system, offers a unique window into these processes, making it invaluable for both study and early diagnosis. This study investigates the impact of the Frontotemporal Dementia-linked IVS 10 + 16 MAPT mutation on retinal development and function using 2D and 3D retinal models derived from human induced pluripotent stem cells.
View Article and Find Full Text PDFRecent advancements in the understanding of the alterations in mitochondrial biogenesis in Alzheimer's disease.
Mol Biol Rep
January 2025
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Raebareli Transit Campus, Bijnour-Sisendi Road, Sarojini Nagar, Lucknow, Uttar Pradesh, 226002, India.
Alzheimer's disease (AD) is a common neurodegenerative disease characterized by progressive memory loss and cognitive decline. The processes underlying the pathophysiology of AD are still not fully understood despite a great deal of research. Since mitochondrial dysfunction affects cellular energy metabolism, oxidative stress, and neuronal survival, it is becoming increasingly clear that it plays a major role in the development of AD.
View Article and Find Full Text PDFNanotechnology in Parkinson's Disease: overcoming drug delivery challenges and enhancing therapeutic outcomes.
Drug Deliv Transl Res
January 2025
Department of Pharmaceutics, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India.
The global prevalence of Parkinson's Disease (PD) is on the rise, driven by an ageing population and ongoing environmental conditions. To gain a better understanding of PD pathogenesis, it is essential to consider its relationship with the ageing process, as ageing stands out as the most significant risk factor for this neurodegenerative condition. PD risk factors encompass genetic predisposition, exposure to environmental toxins, and lifestyle influences, collectively increasing the chance of PD development.
View Article and Find Full Text PDFaux orchestrates the phosphorylation-dependent assembly of the lysosomal V-ATPase in glia and contributes to SNCA/α-synuclein degradation.
Autophagy
January 2025
School of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Glia contribute to the neuropathology of Parkinson disease (PD), but how they react opposingly to be beneficial or detrimental under pathological conditions, like promoting or eliminating SNCA/α-syn (synuclein alpha) inclusions, remains elusive. Here we present evidence that aux (auxilin), the homolog of the PD risk factor GAK (cyclin G associated kinase), regulates the lysosomal degradation of SNCA/α-syn in glia. Lack of glial GAK/aux increases the lysosome number and size, regulates lysosomal acidification and hydrolase activity, and ultimately blocks the degradation of substrates including SNCA/α-syn.
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