acetylglucosamine has been researched along with Memory Disorders in 4 studies
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 4 (100.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Alonso, J; Brooks, SP; Heck, AJR; Hills, R; Leney, AC; McCrimmon, RJ; McNeilly, AD; McWilliams, TG; Muha, V; Read, KD; Schimpl, M; Sutherland, C; van Aalten, DMF; Williamson, R | 1 |
| Hwang, H; Rhim, H | 1 |
| Chu, D; Dai, CL; Gong, CX; Gu, J; Gu, JH; Iqbal, K; Jin, N; Liu, F; Shi, J; Sun, J; Xie, S; Zhang, L | 1 |
| Hsieh-Wilson, LC; Jensen, EH; Rexach, JE; Vinters, HV; Wang, AC | 1 |
4 other study(ies) available for acetylglucosamine and Memory Disorders
| Article | Year |
|---|---|
Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice.
Topics: Acetylglucosamine; Aging; Amino Acid Sequence; Animals; Cell Line; Cognition; Exploratory Behavior; Female; Gene Knock-In Techniques; Humans; Intercellular Signaling Peptides and Proteins; Male; Memory Disorders; Memory, Short-Term; Mice; Mice, Inbred C57BL; Nerve Tissue Proteins; Point Mutation; Protein Processing, Post-Translational | 2019 |
Acutely elevated O-GlcNAcylation suppresses hippocampal activity by modulating both intrinsic and synaptic excitability factors.
Topics: Acetylglucosamine; Animals; beta-N-Acetylhexosaminidases; CA1 Region, Hippocampal; Cells, Cultured; Cognitive Dysfunction; Excitatory Postsynaptic Potentials; Humans; Intravital Microscopy; Male; Memory Disorders; Mice; Models, Animal; N-Acetylglucosaminyltransferases; Neurons; Optical Imaging; Patch-Clamp Techniques; Potassium Channels, Voltage-Gated; Primary Cell Culture; Protein Processing, Post-Translational; Pyrans; Rats; Receptors, AMPA; Synapses; Thiazoles; Voltage-Gated Sodium Channels | 2019 |
O-GlcNAcylation of protein kinase A catalytic subunits enhances its activity: a mechanism linked to learning and memory deficits in Alzheimer's disease.
Topics: Acetylglucosamine; Alzheimer Disease; Animals; Brain; Cyclic AMP Response Element-Binding Protein; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits; Diazooxonorleucine; Down-Regulation; Glycosylation; HEK293 Cells; HeLa Cells; Humans; Learning; Male; Memory; Memory Disorders; Mice, Inbred C57BL; Phosphorylation; Protein Transport; Rats, Sprague-Dawley; Subcellular Fractions; tau Proteins | 2016 |
Loss of O-GlcNAc glycosylation in forebrain excitatory neurons induces neurodegeneration.
Topics: Acetylglucosamine; Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain Mapping; Crosses, Genetic; Female; Glycosylation; Hippocampus; Humans; Inflammation; Male; Memory Disorders; Mice; Mice, Inbred C57BL; Mice, Knockout; N-Acetylglucosaminyltransferases; Neurodegenerative Diseases; Neuroglia; Neurons; Phosphorylation; Prosencephalon; Signal Transduction; tau Proteins | 2016 |