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Epigenetic Regulation

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...

Epigenetic Regulation

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

Epigenetic Regulation

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

Neural Regulation

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.

Parkinson Disease ll: Pathophysiology

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...

Alzheimer Disease ll: Pathophysiology

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

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Related Experiment Video

Updated: May 14, 2026

Characterizing Histone Post-translational Modification Alterations in Yeast Neurodegenerative Proteinopathy Models

Characterizing Histone Post-translational Modification Alterations in Yeast Neurodegenerative Proteinopathy Models

Published on: March 24, 2019

[Neurodegeneration and epigenetics].

Atsushi Iwata¹

¹Department of Molecular Neuroscience on Neurodegeneration, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. iwata-tky@umin.ac.jp

Nihon Shinkei Seishin Yakurigaku Zasshi = Japanese Journal of Psychopharmacology

|February 5, 2013

Summary

This summary is machine-generated.

Epigenetic changes in the Alpha-synuclein (SNCA) gene, specifically CpG methylation, are linked to Parkinson's disease (PD) pathogenesis. Decreased methylation in the substantia nigra of PD patients suggests a novel regulatory mechanism influencing SNCA expression.

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The Detection of 5-Hydroxymethylcytosine in Neural Stem Cells and Brains of Mice

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The Detection of 5-Hydroxymethylcytosine in Neural Stem Cells and Brains of Mice

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Published on: September 19, 2019

Area of Science:

Neuroscience
Genetics
Epigenetics

Context:

Alpha-synuclein (SNCA) gene expression is a key factor in Parkinson's disease (PD) development.
Both genetic mutations (multiplication) and promoter variations influencing SNCA expression are implicated in inherited and sporadic PD.
Epigenetic modifications, such as CpG methylation, are potential regulators of SNCA expression.

Purpose:

To investigate the role of CpG methylation in the SNCA gene promoter region in Parkinson's disease pathogenesis.
To identify specific CpG methylation patterns associated with altered SNCA expression in PD.

Summary:

Researchers identified a specific region within the SNCA CpG island where methylation status correlated with SNCA expression levels in cell cultures.
Postmortem brain analyses revealed non-specific methylation differences in the anterior cingulate and putamen between controls and PD patients.
Significantly decreased methylation was observed in the substantia nigra of PD patients, suggesting a region-specific epigenetic regulation of SNCA.

Impact:

The study suggests a novel epigenetic regulatory mechanism involving SNCA gene methylation that influences Parkinson's disease pathogenesis.
This finding could open new avenues for understanding and potentially targeting epigenetic factors in PD treatment strategies.