Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from Tg4510 and Wild-type mice after AAVTFEB injection

ABSTRACT: We used microarrays to detail the global programme of gene expression after 4 months of TFEB overexpression in the brain. Groups of Tg4510 and Wild-type mice were injected at P0 in the brain. Those groups of mice and the respectively controls were sacrificed and analyzed after 4 months from the injection. RNA extraction from the hippocampus and hybridization on Affymetrix microarrays was done.

ORGANISM(S): Mus musculus

SUBMITTER: Horatiu Voicu

PROVIDER: E-GEOD-53480 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Selective clearance of aberrant tau proteins and rescue of neurotoxicity by transcription factor EB.

Polito Vinicia A VA Li Hongmei H Martini-Stoica Heidi H Wang Baiping B Yang Li L Xu Yin Y Swartzlander Daniel B DB Palmieri Michela M di Ronza Alberto A Lee Virginia M-Y VM Sardiello Marco M Ballabio Andrea A Zheng Hui H

EMBO molecular medicine 20140901 9

Accumulating evidence implicates impairment of the autophagy-lysosome pathway in Alzheimer's disease (AD). Recently discovered, transcription factor EB (TFEB) is a molecule shown to play central roles in cellular degradative processes. Here we investigate the role of TFEB in AD mouse models. In this study, we demonstrate that TFEB effectively reduces neurofibrillary tangle pathology and rescues behavioral and synaptic deficits and neurodegeneration in the rTg4510 mouse model of tauopathy with no ...[more]

PMID: 25069841

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Project description:Extracellular senile plaques of amyloid beta (Abeta) are a pathological hallmark in brain of patients with Alzheimer`s Disease (AD). Abeta is generated by the amyloidogenic processing of the amyloid precursor protein (APP). Concomitant to Abeta load, AD brain is characterized by an increase in protein level and activity of the angiotensin-converting enzyme (ACE). ACE inhibitors are a widely used class of drugs with established benefits for patients with cardiovascular disease. However, the role of ACE and ACE inhibition in the development of Abeta plaques and the process of AD-related neurodegeneration is not clear since ACE was reported to degrade Abeta. To investigate the effect of ACE inhibition on AD-related pathomechanisms, we used Tg2576 mice with neuron-specific expression of APPSwe as AD model. From 12 months of age, substantial Abeta plaque load accumulates in the hippocampus of Tg2576 mice as a brain region, which is highly vulnerable to AD-related neurodegeneration. The effect of central ACE inhibition was studied by treatment of 12 month-old Tg2576 mice for six months with the brain penetrating ACE inhibitor captopril. At an age of 18 months, hippocampal gene expression profiling was performed of captopril-treated Tg2576 mice relative to untreated 18 month-old Tg2576 controls with high Abeta plaque load. As an additional control, we used 12 month-old Tg2576 mice with low Abeta plaque load. Whole genome microarray gene expression profiling revealed gene expression changes induced by the brain-penetrating ACE inhibitor captopril, which could reflect the neuro-regenerative potential of central ACE inhibition. Microarray gene expression profiling was performed of hippocampi isolated from aged, 18 month-old Tg2576 (APPSwe-transgenic) AD mice with high Abeta plaque load relative to age-matched Tg2576 mice, which were treated for 6 months with the centrally active ACE inhibitor captopril. Another study group consisted of 12 month-old Tg2576 mice with low Abeta plaque load. In total, three study groups were analyzed, i.e. (i) 18 month-old untreated Tg2576 mice with high Abeta plaque load, (ii) age-matched Tg2576 mice treated for 6 months with the brain-penetrating ACE inhibitor captopril (20 mg/kg body weight/day in drinking water), and (iii) untreated 12 month-old Tg2576 mice with low Abeta plaque load reflecting the time point when captopril treatment was initiated. Two biological replicates were made of each group, and total hippocampal RNA of four mice was pooled for one gene chip.

Dataset Information

Expression data from Tg4510 and Wild-type mice after AAVTFEB injection

Publications

Selective clearance of aberrant tau proteins and rescue of neurotoxicity by transcription factor EB.

Similar Datasets

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