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Sphingolipid Control of Neural Circuits Via Glial Catabolism.
内容资讯
Sphingolipid Control of Neural Circuits Via Glial Catabolism.
자료유형  
 학위논문
Control Number  
0017164289
International Standard Book Number  
9798342136297
Dewey Decimal Classification Number  
500
Main Entry-Personal Name  
Vaughen, John Philip.
Publication, Distribution, etc. (Imprint  
[S.l.] : Stanford University., 2024
Publication, Distribution, etc. (Imprint  
Ann Arbor : ProQuest Dissertations & Theses, 2024
Physical Description  
119 p.
General Note  
Source: Dissertations Abstracts International, Volume: 86-04, Section: B.
General Note  
Advisor: Clandinin, Thomas R.
Dissertation Note  
Thesis (Ph.D.)--Stanford University, 2024.
Summary, Etc.  
요약Sphingolipids are critical amphipathic molecules present in all eukaryotic cell membranes that are enriched in the developing and adult brain. Though strongly implicated in most neurological diseases, how sphingolipids function in and between brain cells in vivo remains largely enigmatic. Here we dissect the brain functions of Glucocerebrosidase (GBA), a conserved lysosomal hydrolase for sphingolipid catabolism, in a Drosophila model. We identify that glia produce GBA for sphingolipid degradation and neural lysosomal function, and demonstrate that glial gba1bknockout causes diurnal protein aggregate formation, sleep loss, and impaired neurite remodeling in a dynamic circadian circuit that grows and shrinks each day. Remarkably, lipidomics targeted across both time and age revealed diurnal fluctuations in sphingolipids during adulthood as well as a unique sphingolipidome during brain development. The developmental sphingolipidome is characterized by glial catabolism and coordinated neural biosynthesis, and developmental sphingolipids dominate adult patterns of substrate accumulation in glial catabolic mutants. The striking compartmentalization of sphingolipid metabolism between glia and neurons likely acts to finetune neuronal structure and function during both development, adult remodeling, and disease.
Subject Added Entry-Topical Term  
Neurodegeneration.
Subject Added Entry-Topical Term  
Membranes.
Subject Added Entry-Topical Term  
Behavior.
Subject Added Entry-Topical Term  
Neurons.
Subject Added Entry-Topical Term  
Homeostasis.
Subject Added Entry-Topical Term  
CRISPR.
Subject Added Entry-Topical Term  
Alzheimer's disease.
Subject Added Entry-Topical Term  
Blood-brain barrier.
Subject Added Entry-Topical Term  
Hydrocarbons.
Subject Added Entry-Topical Term  
Regulation.
Subject Added Entry-Topical Term  
Pacemakers.
Subject Added Entry-Topical Term  
Disease.
Subject Added Entry-Topical Term  
Biosynthesis.
Subject Added Entry-Topical Term  
Mutation.
Subject Added Entry-Topical Term  
Carbon.
Subject Added Entry-Topical Term  
Cholesterol.
Subject Added Entry-Topical Term  
Brain.
Subject Added Entry-Topical Term  
Insects.
Subject Added Entry-Topical Term  
Metabolism.
Subject Added Entry-Topical Term  
Circadian rhythm.
Subject Added Entry-Topical Term  
Lipids.
Subject Added Entry-Topical Term  
Bioengineering.
Subject Added Entry-Topical Term  
Bioinformatics.
Subject Added Entry-Topical Term  
Neurosciences.
Subject Added Entry-Topical Term  
Physiology.
Added Entry-Corporate Name  
Stanford University.
Host Item Entry  
Dissertations Abstracts International. 86-04B.
Electronic Location and Access  
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Control Number  
joongbu:657668
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