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Antisense directed against PS-1 gene decreases brain oxidative markers in aged senescence accelerated mice (SAMP8) and reverses learning and memory impairment: a proteomics study.

ABSTRACT: Amyloid ?-peptide (A?) plays a central role in the pathophysiology of Alzheimer's disease (AD) through the induction of oxidative stress. This peptide is produced by proteolytic cleavage of amyloid precursor protein (APP) by the action of ?- and ?-secretases. Previous studies demonstrated that reduction of A?, using an antisense oligonucleotide (AO) directed against the A? region of APP, reduced oxidative stress-mediated damage and prevented or reverted cognitive deficits in senescence-accelerated prone mice (SAMP8), a useful animal model for investigating the events related to A? pathology and possibly to the early phase of AD. In the current study, aged SAMP8 were treated by AO directed against PS-1, a component of the ?-secretase complex, and tested for learning and memory in T-maze foot shock avoidance and novel object recognition. Brain tissue was collected to identify the decrease of oxidative stress and to evaluate the proteins that are differently expressed and oxidized after the reduction in free radical levels induced by A?. We used both expression proteomics and redox proteomics approaches. In brain of AO-treated mice a decrease of oxidative stress markers was found, and the proteins identified by proteomics as expressed differently or nitrated are involved in processes known to be impaired in AD. Our results suggest that the treatment with AO directed against PS-1 in old SAMP8 mice reverses learning and memory deficits and reduces A?-mediated oxidative stress with restoration to the normal condition and identifies possible pharmacological targets to combat this devastating dementing disease.

SUBMITTER: Fiorini A

PROVIDER: S-EPMC3855183 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature

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Antisense directed against PS-1 gene decreases brain oxidative markers in aged senescence accelerated mice (SAMP8) and reverses learning and memory impairment: a proteomics study.

Fiorini Ada A Sultana Rukhsana R Förster Sarah S Perluigi Marzia M Cenini Giovanna G Cini Chiara C Cai Jian J Klein Jon B JB Farr Susan A SA Niehoff Michael L ML Morley John E JE Kumar Vijaya B VB Butterfield D Allan DA

Free radical biology & medicine 20130615

Amyloid β-peptide (Aβ) plays a central role in the pathophysiology of Alzheimer's disease (AD) through the induction of oxidative stress. This peptide is produced by proteolytic cleavage of amyloid precursor protein (APP) by the action of β- and γ-secretases. Previous studies demonstrated that reduction of Aβ, using an antisense oligonucleotide (AO) directed against the Aβ region of APP, reduced oxidative stress-mediated damage and prevented or reverted cognitive deficits in senescence-accelerat ...[more]

PMID: 23777706

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Project description:Although the benefits of the consumption of green tea and its components, including catechins and theanine, regarding aging, memory impairment and age-related cognitive decline have been investigated in senescence-accelerated prone mice (SAMP8), studies that simultaneously measured the kinds of proteins that vary in their expression due to the administration of green tea and its extracts were not found. In this study, the effect of dietary and decaffeinated matcha on protein expression in the hippocampus of SAMP 8 was examined comprehensively, mainly using proteomics. Although improvements in memory and the hair appearance of the back coat were limited upon administering the samples, the following regulations were observed in some of the proteins involved in neuron degeneration, Parkinson’s and Alzheimer’s diseases, synapse transmission and nerve cell plasticity, antioxidation, glutamate transport and metabolism, GABA (γ-amino butyric acid) formation and transport and excitatory amino acid transporters: proteins downregulated upon sample intake (p < 0.05): brain acid-soluble protein 1, microtubule-associated protein tau, synapsin-2, sodium- and chloride-dependent GABA transporter; proteins that tended to decrease upon sample intake (0.05 < p < 0.10): Parkinson’s disease (autosomal recessive and early-onset) 7 and synapsin-1; proteins upregulated upon sample intake (p > 0.95): glutathione S-transferase Mu 1, tubulin alpha-1A chain, dynamin-2, calcium/calmodulin-dependent protein kinase type II subunit gamma and tyrosine 3-monooxygenase/tyrosine 5-monooxygenase activation protein epsilon polypeptide; proteins that tended to increase upon sample intake (0.95 > p > 0.90): glutathione S-transferase Mu7 and soluble carrier family 1 (glial high-affinity glutamate transporter); proteins that tended to decrease: sodium- and chloride-dependent GABA transporter 3. These results indicate that matcha and decaffeinated matcha could reduce aging and cognitive impairment by regulating the expression of these proteins. Furthermore, these proteins could be used as markers for the evaluation of food and its available components for reducing aging and cognitive impairment.

Dataset Information

Antisense directed against PS-1 gene decreases brain oxidative markers in aged senescence accelerated mice (SAMP8) and reverses learning and memory impairment: a proteomics study.

Publications

Antisense directed against PS-1 gene decreases brain oxidative markers in aged senescence accelerated mice (SAMP8) and reverses learning and memory impairment: a proteomics study.

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