A Synthetic Pro-Drug Peptide Reverses Amyloid-β-Induced Toxicity in the Rat Model of Alzheimer’s Disease

2019 ◽  
Vol 69 (2) ◽  
pp. 499-512 ◽  
Author(s):  
Sourav Kumar ◽  
Saurabh Srivastav ◽  
Mahino Fatima ◽  
Rajat Subhra Giri ◽  
Bhubaneswar Mandal ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Amyloid Β ◽  
Model Of Alzheimer’S Disease

Time-dependent effect of oligomeric amyloid-β (1–42)-induced hippocampal neurodegeneration in rat model of Alzheimer’s disease

2018 ◽  
Vol 41 (2) ◽  
pp. 139-150 ◽  
Author(s):  
Chennakesavan Karthick ◽  
Saravanan Nithiyanandan ◽  
Musthafa Mohamed Essa ◽  
Gilles J Guillemin ◽  
Swaminathan K Jayachandran ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Amyloid Β ◽  
Time Dependent ◽  
Dependent Effect ◽  
Model Of Alzheimer’S Disease ◽  
Time Dependent Effect ◽  
Hippocampal Neurodegeneration

Daily oscillation of cognitive factors is modified in the temporal cortex of an amyloid β(1-42)-induced rat model of Alzheimer’s disease

2021 ◽  
Vol 170 ◽  
pp. 106-114
Author(s):  
Cinthia Coria-Lucero ◽  
Carina Ledezma ◽  
Andrea Castro ◽  
Silvia Delgado ◽  
Ana Cecilia Anzulovich ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Temporal Cortex ◽  
Amyloid Β ◽  
Cognitive Factors ◽  
Model Of Alzheimer’S Disease ◽  
Daily Oscillation

scholarly journals Neuronal and Astrocytic Metabolism in a Transgenic Rat Model of Alzheimer's Disease

2014 ◽  
Vol 34 (5) ◽  
pp. 906-914 ◽  
Author(s):  
Linn Hege Nilsen ◽  
Menno P Witter ◽  
Ursula Sonnewald
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontal Cortex ◽  
Rat Model ◽  
Hippocampal Formation ◽  
Tricarboxylic Acid Cycle ◽  
Amyloid Β ◽  
Transgenic Rat ◽  
Resonance Spectroscopy ◽  
Model Of Alzheimer’S Disease

Regional hypometabolism of glucose in the brain is a hallmark of Alzheimer's disease (AD). However, little is known about the specific alterations of neuronal and astrocytic metabolism involved in homeostasis of glutamate and GABA in AD. Here, we investigated the effects of amyloid β (Aβ) pathology on neuronal and astrocytic metabolism and glial-neuronal interactions in amino acid neurotransmitter homeostasis in the transgenic McGill-R-Thyl-APP rat model of AD compared with healthy controls at age 15 months. Rats were injected with [1-13C]glucose and [1,2-13C]acetate, and extracts of the hippocampal formation as well as several cortical regions were analyzed using 1H- and 13C nuclear magnetic resonance spectroscopy and high-performance liquid chromatography. Reduced tricarboxylic acid cycle turnover was evident for glutamatergic and GABAergic neurons in hippocampal formation and frontal cortex, and for astrocytes in frontal cortex. Pyruvate carboxylation, which is necessary for de novo synthesis of amino acids, was decreased and affected the level of glutamine in hippocampal formation and those of glutamate, glutamine, GABA, and aspartate in the retrosplenial/cingulate cortex. Metabolic alterations were also detected in the entorhinal cortex. Overall, perturbations in energy- and neurotransmitter homeostasis, mitochondrial astrocytic and neuronal metabolism, and aspects of the glutamate-glutamine cycle were found in McGill-R-Thy1-APP rats.

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