Epigenetic modifications are the cause of memory loss in Alzheimer’s disease

Dementia is the common sequelae of age-related Alzheimer’s disease. This would probably occur due to epigenetic failure. As we know, Alzheimer’s disease is a progressive disorder that causes brain cells to degenerate. It further disrupts cognitive thinking and impairs the behavioral skills of humans.

The molecular underpinning showed that the condition changes the gene expression in the prefrontal cortex. This is the place in the brain associated with social and cognitive thinking. Researchers tried to reverse the condition by inhibiting the harmful gene transcription. They have conducted studies on mouse models and found that the drugs made to inhibit such activity, would help to restore normal gene function. Also, this will favor the neuronal function at ages.

Histone modification

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It is a covalent post-translational modification to histone proteins, that is essential for regulating gene expression. It includes methylation, acetylation, phosphorylation, ubiquitylation, and sumoylation. Histone proteins act to package DNA which wraps around the eight histones, into the chromosome. Above all, the nature of packaging determines whether the genes are either upregulated or suppressed.

Scientists identified H3K4me3, a histone modification, elevated in the prefrontal lobe of AD. Precisely, we can say that modification as histone trimethylation at the amino acid lysine 4. This epigenetic change increases the gene transcription, which leads to the production of more histone-modifying enzymes. And so, while targeting those unnecessary enzymes by the selective drugs, we can possibly have an apt treatment for ADs.

Besides, the researchers found some gene targets, which would get affected by epigenetics. One among is Sgk1, where its level is higher in AD patients. Also, it helps in the opening of ion channels and mediates the action of other hormone releases. Interestingly, the methylation of Sgk1 increases the chance of cellular death in other disease manifestations like Parkinson’s, amyotrophic lateral sclerosis. In conclusion, we can administer a specific Sgk1 inhibitor to decrease the level of tau protein, and also treat the AD patients.

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Source: MedicalXpress

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