Material Type  

 학위논문

 

0017164289

Date and Time of Latest Transaction  

20250211152943

ISBN  

9798342136297

DDC  

500

Author  

Vaughen, John Philip.

Title/Author  

Sphingolipid Control of Neural Circuits Via Glial Catabolism.

Publish Info  

[S.l.] : Stanford University., 2024

Publish Info  

Ann Arbor : ProQuest Dissertations & Theses, 2024

Material Info  

119 p.

General Note  

Source: Dissertations Abstracts International, Volume: 86-04, Section: B.

General Note  

Advisor: Clandinin, Thomas R.

학위논문주기  

Thesis (Ph.D.)--Stanford University, 2024.

Abstracts/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