Combined administration of D-galactose and aluminium induces Alzheimerlike lesions in brain

Xiao, Fei; Xiao-guang, LI; Zhang, Xiaoyu; Hou, Jun-Dai; Liu, Lin; Gao, Qin; Luo, Hongyu

doi:10.1007/s12264-011-1028-2

Cited by 81 publications

(55 citation statements)

References 22 publications

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“…The combined administration of aluminum (20 mg/kg, intragastrically, once per day) and d -galactose (120 mg/kg, injected subcutaneously, once per day) has been shown to decrease the whole-brain ACh level and activities of ChAT and AChE in mice after treatment for 10 weeks [13]. However, we detected no significant alteration in ACh level or the activity of ChAT or AChE in the cerebral cortex of AD-like mice.…”

Section: Resultscontrasting

confidence: 60%

“…The Morris water maze is commonly used to test hippocampal-dependent spatial learning and memory. Morris water maze results from a previous study and ours showed impaired spatial memory in AD-like mice subjected to combined d -galactose and aluminum treatment [13,14]. In this study, step-down-type passive avoidance tests conducted to investigate non-spatial long-term memory demonstrated reduced cognitive function in AD-like mice.…”

Section: Resultssupporting

confidence: 57%

“…In this study, mice with AD-like lesions induced by the combined administration of aluminum and d -galactose [13] were used to investigate the anti-AD effects of SFN. SFN ameliorated cognitive impairment and attenuated cholinergic neuron loss in the MS and hippocampal CA1 regions in AD-like mice.…”

Section: Resultsmentioning

confidence: 99%

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Neuroprotective Effects of Sulforaphane on Cholinergic Neurons in Mice with Alzheimer’s Disease-Like Lesions

Zhang

Fang

et al. 2014

IJMS

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Alzheimer’s disease (AD) is a common neurodegenerative disease in elderly individuals, and effective therapies are unavailable. This study was designed to investigate the neuroprotective effects of sulforaphane (an activator of NF-E2-related factor 2) on mice with AD-like lesions induced by combined administration of aluminum and d-galactose. Step-down-type passive avoidance tests showed sulforaphane ameliorated cognitive impairment in AD-like mice. Immunohistochemistry results indicated sulforaphane attenuated cholinergic neuron loss in the medial septal and hippocampal CA1 regions in AD-like mice. However, spectrophotometry revealed no significant difference in acetylcholine level or the activity of choline acetyltransferase or acetylcholinesterase in the cerebral cortex among groups of control and AD-like mice with and without sulforaphane treatment. Sulforaphane significantly increased the numbers of 5-bromo-2'-deoxyuridine-positive neurons in the subventricular and subgranular zones in AD-like mice which were significantly augmented compared with controls. Atomic absorption spectrometry revealed significantly lower aluminum levels in the brains of sulforaphane-treated AD-like mice than in those that did not receive sulforaphane treatment. In conclusion, sulforaphane ameliorates neurobehavioral deficits by reducing cholinergic neuron loss in the brains of AD-like mice, and the mechanism may be associated with neurogenesis and aluminum load reduction. These findings suggest that phytochemical sulforaphane has potential application in AD therapeutics.

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Section: Resultscontrasting

confidence: 60%

Section: Resultssupporting

confidence: 57%

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Neuroprotective Effects of Sulforaphane on Cholinergic Neurons in Mice with Alzheimer’s Disease-Like Lesions

Zhang

Fang

et al. 2014

IJMS

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“…ACh is synthesized by the ChAT-catalyzed reaction of choline with acetoacetyl-CoA and resolved by AChE. ChAT and AChE together maintain the dynamic balance of ACh (22). AChE has high catalytic activity and inactivates ACh by resolving it into choline and acetic acid to ensure effective transfer at the cholinergic nerve.…”

Section: Discussionmentioning

confidence: 99%

Expression of APP, BACE1, AChE and ChAT in an AD model in rats and the effect of donepezil hydrochloride treatment

Chen

Liu

et al. 2012

Molecular Medicine Reports

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Abstract. The aim of this study was to investigate the pathological changes in a rat model of Alzheimer's disease (AD) and the effect of donepezil hydrochloride (HCl) treatment. The rat model of AD was established by the bilateral injection of amyloid β 1-40 (Aβ 1-40 ) into the hippocampus. Changes in spatial learning and memory functions were examined using the Morris water maze test and changes in catalase (CAT) and glutathione peroxidase (GSH-Px) activities were determined using chemical colorimetry. Moreover, the changes in acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) expression were analyzed using immunohistochemical staining. The mRNA expression levels of the amyloid precursor protein (APP) and β-secreted enzyme 1 (BACE1) were evaluated using RT-PCR. The effects of donepezil HCl on the aforementioned indices were also observed. The rat memories of the platform quadrants in the blank, sham and donepezil HCl groups were improved compared with those of the rats in the model group. The ratio of swim distance in the fourth platform quadrant (l 4 ) to the total swim distance (l total) for the model group rats (l 4 /l total) was significantly decreased compared with that for the blank and sham group rats. Following donepezil HCl treatment, the ratio of l 4 /l total significantly increased. AD modeling caused a significant decrease in the CAT and GSH-Px activities in the brain tissues of the rats. The CAT and GSH-Px activities in the AD model rats significantly increased following donepezil HCl treatment. Moreover, donepezil HCl treatment significantly decreased the AChE, APP and BACE1 mRNA expression levels and increased the ChAT expression levels. Therefore, donepezil HCl was able to significantly decrease learning and memory damage in a rat model of AD.

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“…And there are studys suggest that D-gal administration disrupts the structural integrity of the neuronal-glial-vascular units (Liu et al, 2010c) and induces brain energy metabolism disturbance (Zhang et al, 2008). Basing on these models, we employed a new model for AD using long-term AlCl 3 and D-galinjection (Luo et al, 2009;Sun et al, 2009;Xiao et al, 2011), which has been extensively used in research to screen for drugs to prevent or reverse AD in china (Feng et al, 2010(Feng et al, , 2009Jiping et al, 2011). The present results suggested that AlCl 3 and D-galcould induce rats' learning and memory impairment, decrease rCBF and cerebral metabolism and affects the expression of ET-1, eNOS and APP mRNA in hippocampus, suggesting that this rat model might be a useful model for studies Alzheimer on cerebral blood flow, the brain metabolism and energetics and the cerebrovascular function.…”

Section: Agmentioning

confidence: 99%

Cerebrovascular protection of β-asarone in Alzheimer's disease rats: A behavioral, cerebral blood flow, biochemical and genic study

Zhao

Qian

et al. 2012

Journal of Ethnopharmacology

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Combined administration of D-galactose and aluminium induces Alzheimerlike lesions in brain

Cited by 81 publications

References 22 publications

Neuroprotective Effects of Sulforaphane on Cholinergic Neurons in Mice with Alzheimer’s Disease-Like Lesions

Neuroprotective Effects of Sulforaphane on Cholinergic Neurons in Mice with Alzheimer’s Disease-Like Lesions

Expression of APP, BACE1, AChE and ChAT in an AD model in rats and the effect of donepezil hydrochloride treatment

Cerebrovascular protection of β-asarone in Alzheimer's disease rats: A behavioral, cerebral blood flow, biochemical and genic study

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