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CLN3 disease disrupts very early postnatal hippocampal maturation
Jeet B. Singh
, Devin M. Burris
, Sangeetha Bhuyan
, Tegan Thurston
, Anna Oschmann
, Connor Jankowski
, Wenyun Lu
,
Joshua D. Rabinowitz
, Rebecca C. Ahrens-Nicklas
Chemistry
High Meadows Environmental Institute
Lewis-Sigler Institute for Integrative Genomics
Molecular Biology
Princeton Branch of the Ludwig Institute for Cancer Research
Research output
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Contribution to journal
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Article
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peer-review
4
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Keyphrases
Early Postnatal
100%
CLN3 Disease
100%
Hippocampus
57%
Early Development
28%
Pathologic
28%
Electroencephalogram
28%
Glycerophospholipids
28%
Hippocampal Circuit
28%
Lysosomal Storage Disease
28%
Mouse Model
14%
Network Level
14%
Metabolism
14%
Brain Regions
14%
Neurodegeneration
14%
Voltage-sensitive Dye Imaging
14%
Excitability
14%
Circuit Function
14%
Hydrophilic Interaction Liquid Chromatography (HILIC)
14%
Liquid Chromatography-high Resolution Mass Spectrometry (LC-HRMS)
14%
Circuit Dynamics
14%
Functional Defects
14%
Disease Pathogenesis
14%
Functional Markers
14%
Model Priors
14%
Neurodevelopment
14%
Biochemical Markers
14%
Atypical Forms
14%
Hippocampal Excitability
14%
Batten Disease
14%
Neurodegenerative Disorders
14%
Juvenile Neuronal Ceroid Lipofuscinosis
14%
Neuroscience
Hippocampus
100%
In Vivo
50%
Excitability
50%
Electroencephalogram
50%
Neuronal Ceroid Lipofuscinosis
50%
In Vitro
25%
Metabolic Pathway
25%
Mass Spectrometry
25%
Neurodegenerative Disorder
25%
Brain Region
25%
Biological Marker
25%
Chromatography
25%
Biochemistry, Genetics and Molecular Biology
Maturation
100%
CLN3
100%
Excitability
28%
Electroencephalogram
28%
Batten Disease
28%
Neuronal Ceroid Lipofuscinosis
28%
Metabolic Pathway
14%
Mouse Model
14%
Voltage-Sensitive Dye
14%
P21
14%
Resolution (Mass Spectrometry)
14%
Hydrophilic Interaction Chromatography
14%