Chronic systemic D‐galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: Protective effects of R‐α‐lipoic acid
@article{Cui2006ChronicSD, title={Chronic systemic D‐galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: Protective effects of R‐$\alpha$‐lipoic acid}, author={Xu Cui and Ping-Ping Zuo and Qing Zhang and Xue-kun Li and Ya-zhuo Hu and Jiangang Long and Lester Packer and Jiankang Liu}, journal={Journal of Neuroscience Research}, year={2006}, volume={84} }
Chronic systemic exposure of mice, rats, and Drosophila to D‐galactose causes the acceleration of senescence and has been used as an aging model. The underlying mechanism is yet unclear. To investigate the mechanisms of neurodegeneration in this model, we studied cognitive function, hippocampal neuronal apoptosis and neurogenesis, and peripheral oxidative stress biomarkers, and also the protective effects of the antioxidant R‐alpha‐lipoic acid. Chronic systemic exposure of D‐galactose (100 mg…
258 Citations
Melatonin improves d‐galactose‐induced aging effects on behavior, neurogenesis, and lipid peroxidation in the mouse dentate gyrus via increasing pCREB expression
- Biology, ChemistryJournal of pineal research
- 2012
It is suggested that melatonin may be helpful in reducing age‐related phenomena in the brain by significantly ameliorating the d‐galactose‐induced increase in escape latency and neuronal damage compared with the vehicle‐treated group.
Melatonin attenuates D‐galactose‐induced memory impairment, neuroinflammation and neurodegeneration via RAGE/NF‐KB/JNK signaling pathway in aging mouse model
- BiologyJournal of pineal research
- 2015
Melatonin acts as a pleiotropic agent in various age‐related neurodegenerative diseases. In this study, we examined the underlying neuroprotective mechanism of melatonin against D‐galactose‐induced…
Pioglitazone alleviates the mitochondrial apoptotic pathway and mito‐oxidative damage in the d‐galactose‐induced mouse model
- BiologyClinical and experimental pharmacology & physiology
- 2013
The present study highlights the protective effects of pioglitzone against d‐galactose‐induced memory dysfunction, mito‐oxidative damage and apoptosis through activation of PPARγ receptors and suggests that pioglitazone might be helpful for the prevention or alleviation of ageing.
Anthocyanins Reversed D-Galactose-Induced Oxidative Stress and Neuroinflammation Mediated Cognitive Impairment in Adult Rats
- Biology, ChemistryMolecular Neurobiology
- 2015
The results suggest that anthocyanins could be a safe and promising anti-oxidant and anti-neuroinflammatory agent for age-related neurodegenerative diseases such as Alzheimer’s disease.
Role of D-galactose-induced brain aging and its potential used for therapeutic interventions
- BiologyExperimental Gerontology
- 2018
Caffeine prevents d-galactose-induced cognitive deficits, oxidative stress, neuroinflammation and neurodegeneration in the adult rat brain
- BiologyNeurochemistry International
- 2015
Glycine, the smallest amino acid, confers neuroprotection against d-galactose-induced neurodegeneration and memory impairment by regulating c-Jun N-terminal kinase in the mouse brain
- BiologyJournal of neuroinflammation
- 2020
Gly (an amino acid) is a safe and promising neurotherapeutic candidate that might be used for age-related neurodegenerative diseases and markedly improved behavioral measures of cognitive deficits in d -gal-treated mice.
D-galactose effectiveness in modeling aging and therapeutic antioxidant treatment in mice.
- BiologyRejuvenation research
- 2010
Results of this study illustrate that chronic, short-term D-galactose treatment may not represent a suitable model for inducing readily detectable age-related neurobehavioral symptoms in mice.
Gintonin Attenuates D-Galactose-Induced Hippocampal Senescence by Improving Long-Term Hippocampal Potentiation, Neurogenesis, and Cognitive Functions
- BiologyGerontology
- 2018
Gintonin administration restores D-gal-induced memory deficits by enhancing hippocampal LPA1 receptor expression, LTP, and neurogenesis and exerts anti-brain aging effects that are responsible for alleviating brain aging-related dysfunction.
Centella asiatica Attenuates D-Galactose-Induced Cognitive Impairment, Oxidative and Mitochondrial Dysfunction in Mice
- BiologyInternational journal of Alzheimer's disease
- 2011
Centella asiatica treatment significantly improved behavioral alterations, oxidative damage and mitochondrial enzyme complex activities as compared to contro l (D-galactose), and attenuated enhanced acetylcholine esterase enzyme level in D-Galactose senescence mice.
References
SHOWING 1-10 OF 53 REFERENCES
Melatonin reduces memory changes and neural oxidative damage in mice treated with D‐galactose
- Biology, PsychologyJournal of pineal research
- 2002
The data suggest that D‐galactose is involved in accelerating the brain aging process by elevating free radical generation and reducing antioxidative enzyme activities in vivo.
D-Galactose injured neurogenesis in the hippocampus of adult mice
- BiologyNeurological research
- 2005
D-Galactose induced the impairment of neurogenesis in the DG, which is similar to natural aging in mice, and ROS accumulation as a result of D-galactose may be related to the decrease of neuro Genetically modified cell proliferation and survival in the dentate gyrus.
Establishment of the mimetic aging effect in mice caused by D-galactose
- BiologyBiogerontology
- 2004
By reference to theoxidative biomarkers in blood, brain and liver, the reliability of mimetic aging model is confirmed and is relative to free radical and the accumulation of waste substances in metabolism.
Advanced glycation in d-galactose induced mouse aging model
- BiologyMechanisms of Ageing and Development
- 1999
Selective impairment of hippocampal neurogenesis by chronic alcoholism: Protective effects of an antioxidant
- Psychology, BiologyProceedings of the National Academy of Sciences of the United States of America
- 2003
The studies indicate that alcohol abuse, even for a short duration, results in the death of newly formed neurons within the adult brain and that the underlying mechanism is related to oxidative or nitrosative stress.
Effects of puerarin on D-galactose-induced memory deficits in mice.
- Biology, ChemistryActa pharmacologica Sinica
- 2002
Compared with the D-galactose control group, puerarin 60 mg/kg was shown to increase significantly the spontaneous behavior and explorative response in the open field and improve remarkably the learning-memory ability of the aging mice induced by D- Galactose.
Mimetic brain aging effect induced by D-galactose in mice
- Biology, Chemistry
- 1995
The mimetic brain aging effect has been induced by D-galactose injection and the results suggest s decreased transcription activity shown by above described parameters except for C-fos mRNA level.
Radiation Response of Neural Precursor Cells: Linking Cellular Sensitivity to Cell Cycle Checkpoints, Apoptosis and Oxidative Stress
- Biology, MedicineRadiation research
- 2004
The temporal coincidence between in vitro and in vivo measurements of apoptosis suggests that oxidative stress may provide a mechanistic explanation for radiation-induced inhibition of neurogenesis in the development of cognitive impairment.
Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: Partial reversal by feeding acetyl-l-carnitine and/or R-α-lipoic acid
- BiologyProceedings of the National Academy of Sciences of the United States of America
- 2002
Accumulation of oxidative damage to mitochondria, protein, and nucleic acid in the brain may lead to neuronal and cognitive dysfunction. The effects on cognitive function, brain mitochondrial…
Ischemia‐induced neurogenesis is preserved but reduced in the aged rodent brain
- Biology, MedicineAging cell
- 2004
It is concluded that ischemia‐induced neurogenesis occurs in the aged brain, and that measures designed to augment this phenomenon might have therapeutic applications.