A Serial Analysis of Gene Expression Profile of the Alzheimer’s Disease Tg2576 Mouse Model

2009 ◽  
Vol 17 (4) ◽  
pp. 360-379 ◽  
Author(s):  
Amee J. George ◽  
Lavinia Gordon ◽  
Tim Beissbarth ◽  
Irene Koukoulas ◽  
R. M. Damian Holsinger ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Tg2576 Mouse

Gene expression profile of the PDAPP mouse model for Alzheimer's disease with and without Apolipoprotein E

2009 ◽  
Vol 30 (4) ◽  
pp. 574-590 ◽  
Author(s):  
Simon P. Selwood ◽  
S. Parvathy ◽  
Barbara Cordell ◽  
Heather S. Ryan ◽  
Farshid Oshidari ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Apolipoprotein E ◽  
Gene Expression Profile ◽  
Expression Profile

P2-137: COMPARISON OF GENE EXPRESSION PROFILE OF ALZHEIMER'S DISEASE USING MODULAR MAXIMIZATION ALGORITHM REVEALS OPPOSING ROLES FOR TGIF AND EGR3

2006 ◽  
Vol 14 (7S_Part_13) ◽  
pp. P720-P720
Author(s):  
Saranya Canchi ◽  
Balaji Raao ◽  
Sara Brin Rosenthal ◽  
Roman Sasik ◽  
Kathleen M. Fisch ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Expression Profile ◽  
Expression Profile

A Gene Expression Profile of Alzheimer's Disease

2001 ◽  
Vol 20 (11) ◽  
pp. 683-695 ◽  
Author(s):  
J.F. Loring ◽  
X. Wen ◽  
J.M. Lee ◽  
J. Seilhamer ◽  
R. Somogyi
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Expression Profile ◽  
Expression Profile

O2-04-07: A Serial Analysis of Gene Expression (SAGE) profile of the Alzheimer's disease TG2576 mouse model

2006 ◽  
Vol 2 ◽  
pp. S39-S39
Author(s):  
Amee J. George ◽  
Lavinia Gordon ◽  
Tim Beissbarth ◽  
Irene Koukoulas ◽  
R.M. Damian Holsinger ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Tg2576 Mouse

P1-053: Gene expression changes related to synaptic deficits in the Tg2576 mouse model of Alzheimer's disease

2008 ◽  
Vol 4 ◽  
pp. T221-T221
Author(s):  
Clark A. Briggs ◽  
David J. Anderson ◽  
Won Choi ◽  
Paul E. Kroeger ◽  
Jinhe Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Tg2576 Mouse ◽  
Model Of Alzheimer’S Disease

scholarly journals Metabolic Profiling of Suprachiasmatic Nucleus Reveals Multifaceted Effects in an Alzheimer’s Disease Mouse Model

2021 ◽  
pp. 1-12
Author(s):  
Muhamed N.H. Eeza ◽  
Rico Singer ◽  
Corinna Höfling ◽  
Jörg Matysik ◽  
Huub J.M. de Groot ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Metabolic Profiling ◽  
Inflammatory Responses ◽  
Immunohistochemical Analysis ◽  
Magic Angle Spinning ◽  
Tg2576 Mouse ◽  
Magic Angle ◽  
Gaba Production

Background: Circadian rhythm disturbance is commonly observed in Alzheimer’s disease (AD). In mammals, these rhythms are orchestrated by the superchiasmatic nucleus (SCN). Our previous study in the Tg2576 AD mouse model suggests that inflammatory responses, most likely manifested by low GABA production, may be one of the underlying perpetrators for the changes in circadian rhythmicity and sleep disturbance in AD. However, the mechanistic connections between SCN dysfunction, GABA modulation, and inflammation in AD is not fully understood. Objective: To reveal influences of amyloid pathology in Tg2576 mouse brain on metabolism in SCN and to identify key metabolic sensors that couple SCN dysfunction with GABA modulation and inflammation. Methods: High resolution magic angle spinning (HR-MAS) NMR in conjunction with multivariate analysis was applied for metabolic profiling in SCN of control and Tg2576 female mice. Immunohistochemical analysis was used to detect neurons, astrocytes, expression of GABA transporter 1 (GAT1) and Bmal1. Results: Metabolic profiling revealed significant metabolic deficits in SCN of Tg2576 mice. Reductions in glucose, glutamate, GABA, and glutamine provide hints toward an impaired GABAergic glucose oxidation and neurotransmitter cycling in SCN of AD mice. In addition, decreased redox co-factor NADPH and glutathione support a redox disbalance. Immunohistochemical examinations showed low expression of the core clock gene, Bmal1, especially in activated astrocytes. Moreover, decreased expression of GAT1 in astrocytes indicates low GABA recycling in this cell type. Conclusion: Our results suggest that redox disbalance and compromised GABA signaling are important denominators and connectors between neuroinflammation and clock dysfunction in AD.

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