Epigenetic mechanisms in the development of memory and their involvement in certain neurological diseases

Rosales-Reynoso, Mónica Alejandra; Ochoa-Hernández, Alejandra Berenice; Juárez-Vázquez, Clara Ibet; Barros‐Núñez, Patricio

doi:10.1016/j.nrleng.2014.02.011

Cited by 6 publications

(4 citation statements)

References 52 publications

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“…Moreover, these data highlight the highly sensitive nature of DNA methylation processes during the early stages of LTP maintenance. In fact, evidence indicates that perturbing epigenetic regulatory mechanisms can have devastating effects on neuronal functions [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of DNA Methylation Impairs Synaptic Plasticity during an Early Time Window in Rats

et al. 2016

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Although the importance of DNA methylation-dependent gene expression to neuronal plasticity is well established, the dynamics of methylation and demethylation during the induction and expression of synaptic plasticity have not been explored. Here, we combined electrophysiological, pharmacological, molecular, and immunohistochemical approaches to examine the contribution of DNA methylation and the phosphorylation of Methyl-CpG-binding protein 2 (MeCP2) to synaptic plasticity. We found that, at twenty minutes after theta burst stimulation (TBS), the DNA methylation inhibitor 5-aza-2-deoxycytidine (5AZA) impaired hippocampal long-term potentiation (LTP). Surprisingly, after two hours of TBS, when LTP had become a transcription-dependent process, 5AZA treatment had no effect. By comparing these results to those in naive slices, we found that, at two hours after TBS, an intergenic region of the RLN gene was hypomethylated and that the phosphorylation of residue S80 of MeCP2 was decreased, while the phosphorylation of residue S421 was increased. As expected, 5AZA affected only the methylation of the RLN gene and exerted no effect on MeCP2 phosphorylation patterns. In summary, our data suggest that tetanic stimulation induces critical changes in synaptic plasticity that affects both DNA methylation and the phosphorylation of MeCP2. These data also suggest that early alterations in DNA methylation are sufficient to impair the full expression of LTP.

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Section: Discussionmentioning

confidence: 99%

Inhibition of DNA Methylation Impairs Synaptic Plasticity during an Early Time Window in Rats

et al. 2016

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“…Despite these obvious differences, the methylation pattern and gene expression profiles of lymphocytes are largely maintained in LCLs and display many of the specific characteristics of primary B cells [ 58 ]. This is also true for many diseases, and clear differences in the transcriptomes and the epigenomes of patients and controls have been identified in LCLs for numerous diseases [ 59 , 60 , 61 , 62 , 63 ]. LCLs are increasingly being used as models of disease and given their high oxidative nature, are ideal systems for studying mitochondrial function.…”

Section: Types Of Human Cellular Disease Modelsmentioning

confidence: 99%

Lymphoblastoid Cell Lines as Models to Study Mitochondrial Function in Neurological Disorders

Annesley

Fisher

2021

IJMS

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Neurological disorders, including neurodegenerative diseases, are collectively a major cause of death and disability worldwide. Whilst the underlying disease mechanisms remain elusive, altered mitochondrial function has been clearly implicated and is a key area of study in these disorders. Studying mitochondrial function in these disorders is difficult due to the inaccessibility of brain tissue, which is the key tissue affected in these diseases. To overcome this issue, numerous cell models have been used, each providing unique benefits and limitations. Here, we focussed on the use of lymphoblastoid cell lines (LCLs) to study mitochondrial function in neurological disorders. LCLs have long been used as tools for genomic analyses, but here we described their use in functional studies specifically in regard to mitochondrial function. These models have enabled characterisation of the underlying mitochondrial defect, identification of altered signalling pathways and proteins, differences in mitochondrial function between subsets of particular disorders and identification of biomarkers of the disease. The examples provided here suggest that these cells will be useful for development of diagnostic tests (which in most cases do not exist), identification of drug targets and testing of pharmacological agents, and are a worthwhile model for studying mitochondrial function in neurological disorders.

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“…La epigenética se podría considerar como una rama de la biología que explica el por qué los organismos vivos expresan unos genes y silencian otros para conformar así sus características físicas y la susceptibilidad de desarrollar determinadas enfermedades. Los mecanismos epigenéticos regulan cómo y en qué grado estas características tienen que expresarse, así el genoma incluye la secuencia completa del ADN y el epigenoma se refiere a los elementos que regulan la expresión de los genes sin alterar la secuencia del ADN (12,13). Por lo anterior se deduce que el genoma no es estático y se puede modificar.…”

Section: Modificaciones Epigenéticas En El Genoma Humanounclassified

Relación epigenética entre la desnutrición materna y la diabetes mellitus tipo 2

2019

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En la actualidad la diabetes mellitus representa un gran problema de salud pública. Su gran prevalencia e incidencia la han puesto como una de las enfermedades crónicas más comunes de los últimos años solo por debajo de la hipertensión arterial, el cáncer y la enfermedad pulmonar obstructiva crónica. Al encontrar evidencia epigenética de la relación entre la desnutrición materna y el desarrollo de la diabetes mellitus tipo dos se logra no solo disminuir la tasa de incidencia de la enfermedad previniendo la desnutrición materna, sino también avanzar en estudios de tratamiento hacia la diana del problema en cuanto a epigenética se discute.

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Epigenetic mechanisms in the development of memory and their involvement in certain neurological diseases

Cited by 6 publications

References 52 publications

Inhibition of DNA Methylation Impairs Synaptic Plasticity during an Early Time Window in Rats

Inhibition of DNA Methylation Impairs Synaptic Plasticity during an Early Time Window in Rats

Lymphoblastoid Cell Lines as Models to Study Mitochondrial Function in Neurological Disorders

Relación epigenética entre la desnutrición materna y la diabetes mellitus tipo 2

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