NEUROEPIGENETICS AND PLASTICITY IN NEURODEGENERATIVE DISEASES

Abstract

Neurodegenerative disorders such as Alzheimer, Parkinson and Huntington result in serious working deficiency of the neurons. The changes in the way synaptic plasticity and gene expression behave, as a rule, cause these problems, and they are not functioning properly.  It is an example of mixed-methods experimental research studies that investigate neuroepigenetic origins of these problems integrating a combination of molecular profiling, electrophysiological tests and expert analysis.  We analyzed crucially regulated markers by chromatin immunoprecipitation sequencing, measure of DNA methylation and protein quantification of rodent models of both types of illness. These were HDACs, BDNF, CREB and MeCP2.  Meanwhile hippocampus slice recording was fulfilled to examine the synaptic plasticity based on LTP and LTD indexes.  The diseased groups possessed significantly higher HDAC and DNA methylation and lower amounts of BDNF and CREB levels as that of controls.  The quantitative research revealed a positive correlation among histone acetylation and plasticity score as well as a negative correlation between the level of HDAC and plasticity score.  What scatterplot and PCA projections demonstrated was that the illness models came together in varying combinations depending on their epigenetic and functional features. The poorest deficiencies in plasticity were recorded in Huntington and Parkinson groups.  The analysis of the interviews with experts supported the idea that targeting epigenetic modifiers can be beneficial in research, when considering the perspective of HDAC inhibitors, and environmental enrichment as an option when it comes to treatment.  The relationships between epigenetic status and neurofunctional outcomes were more evident due to figures of expression profile, synaptic index, correlation matrix and PCA.  The combination of these outcomes gives convincing evidence regarding the role of neuroepigenetic control in the making of synapses strong or weak in neurodegenerative disease conditions.  This work contributes to our understanding of the mechanics behind neurodegenerative diseases as well as how these diseases can be treated because it highlights specific epigenetic pathways that can be altered to interrupt the pathology of neurodegenerative diseases.