Analysis of SNAP25 mRNA expression and promoter DNA methylation in brain areas of Alzheimer’s Disease patients

Furuya, Tatiane Katsue; Silva, P. N. O.; Payão, Spencer Luíz Marques; Bertolucci, Paulo Henrique Ferreira; Rasmussen, Lucas Trevizani; Lábio, Roger Willian de; Braga, I.; Chen, Elizabeth; Turecki, Gustavo; Mechawar, Naguib; Mill, Jonathan; Smith, Marı́lia de Arruda Cardoso

doi:10.1016/j.neuroscience.2012.06.035

Cited by 46 publications

(27 citation statements)

References 28 publications

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“…APOE genotype correlates with synaptosomal-associated protein 25 (SNAP25) depletion in frontotemporal lobar degeneration (Connelly et al, 2011), which showed decreased expression in CCH rat synapses. Clinical data has already described the reduced level of SNAP25 protein in AD suggesting its role in impaired neurotransmission (Furuya et al, 2012), which was also strengthened by the fact that single nucleotide polymorphisms are associated with functional MRI parameters in AD (Guerini et al, 2014). SNAP25 increases the surface expression of sodium-and chloride-dependent GABA transporter 1 (SLC6A1) (Fan et al, 2006).…”

Section: Apoe-mediated Synaptic Effects Of Chronic Cerebral Hypoperfumentioning

confidence: 94%

Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex

et al. 2017

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Chronic cerebral hypoperfusion (CCH) evokes mild cognitive impairment (MCI) and contributes to the progression of vascular dementia and Alzheimer's disease (AD). How CCH 2 induces these neurodegenerative processes that may spread along the synaptic network and whether they are detectable at the synaptic proteome level of the cerebral cortex remains to be established.In the present study, we report the synaptic protein changes in the cerebral cortex after stepwise bilateral common carotid artery occlusion (BCCAO) induced CCH in the rat. The occlusions were confirmed with Magnetic Resonance Angiography 5 weeks after the surgery.Synaptosome fractions were prepared using sucrose gradient centrifugation from cerebral cortex dissected 7 weeks after the occlusion. The synaptic protein differences between the sham operated and CCH groups were analysed with label free nanoUHPLC-MS/MS.

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Section: Apoe-mediated Synaptic Effects Of Chronic Cerebral Hypoperfumentioning

confidence: 94%

Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex

et al. 2017

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“…These genes include synaptosomal-associated protein 25 ( SNAP-25 ) (Furuya et al, 2012b), SIRT3 , SMARCA5 , CDH1 (Silva et al, 2008), 2′,3′-cyclic-nucleotide 3′-phosphodiesterase ( CNP ), and dihydropyrimidinase-like 2 ( DPYSL2 ) (Silva et al, 2013). …”

Section: Dna Methylation and Alzheimer's Diseasementioning

confidence: 99%

DNA methylation, a hand behind neurodegenerative diseases

Lu¹,

Liu²,

Y³

et al. 2013

Front. Aging Neurosci.

145

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Epigenetic alterations represent a sort of functional modifications related to the genome that are not responsible for changes in the nucleotide sequence. DNA methylation is one of such epigenetic modifications that have been studied intensively for the past several decades. The transfer of a methyl group to the 5 position of a cytosine is the key feature of DNA methylation. A simple change as such can be caused by a variety of factors, which can be the cause of many serious diseases including several neurodegenerative diseases. In this review, we have reviewed and summarized recent progress regarding DNA methylation in four major neurodegenerative diseases: Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). The studies of these four major neurodegenerative diseases conclude the strong suggestion of the important role DNA methylation plays in these diseases. However, each of these diseases has not yet been understood completely as details in some areas remain unclear, and will be investigated in future studies. We hope this review can provide new insights into the understanding of neurodegenerative diseases from the epigenetic perspective.

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“…AD is a neurological disorder, which is the most prevalent form of age‐related dementia in modern society. AD causes synaptic loss in specific brain regions, such as in the cortex and hippocampus . Neurofibrillary tangles, dystrophic neuritis and amyloid‐β deposits characterize AD.…”

Section: Dna Methylation In Mammalian Disordersmentioning

confidence: 99%

“…AD causes synaptic loss in specific brain regions, such as in the cortex and hippocampus. 82,83 Neurofibrillary tangles, dystrophic neuritis and amyloid-β deposits characterize AD. AD is also associated with increased activation of apoptosis pathways, mitochondrial dysfunction, oxidative stress and DNA damage that lead to synaptic defects resulting in neuronal death.…”

Section: Dna Methylation In Neurodegenerative Disordersmentioning

confidence: 99%

DNA methylation dynamics in plants and mammals: overview of regulation and dysregulation

Elhamamsy

2016

Cell Biochemistry & Function

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DNA methylation is a major epigenetic marking mechanism regulating various biological functions in mammals and plant. The crucial role of DNA methylation has been observed in cellular differentiation, embryogenesis, genomic imprinting and X-chromosome inactivation. Furthermore, DNA methylation takes part in disease susceptibility, responses to environmental stimuli and the biodiversity of natural populations. In plant, different types of environmental stress have demonstrated the ability to alter the archetype of DNA methylation through the genome, change gene expression and confer a mechanism of adaptation. DNA methylation dynamics are regulated by three processes de novo DNA methylation, methylation maintenance and DNA demethylation. These processes have their similarities and differences between mammals and plants. Furthermore, the dysregulation of DNA methylation dynamics represents one of the primary molecular mechanisms of developing diseases in mammals. This review discusses the regulation and dysregulation of DNA methylation in plants and mammals. Copyright © 2016 John Wiley & Sons, Ltd.

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Analysis of SNAP25 mRNA expression and promoter DNA methylation in brain areas of Alzheimer’s Disease patients

Cited by 46 publications

References 28 publications

Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex

Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex

DNA methylation, a hand behind neurodegenerative diseases

DNA methylation dynamics in plants and mammals: overview of regulation and dysregulation

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