Wednesday January 22, 2020

It is Now Possible to Reverse Memory Loss Caused by Alzheimer’s, Says Study

Future studies will focus on developing compounds that penetrate the brain more effectively and are thus longer-lasting, the researchers said

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In Alzheimer's disease, patients start losing memory. Pixabay

Researchers have developed a novel approach that may one day make it possible to reverse memory loss, caused by Alzheimer’s disease.

The team, led by University at Buffalo scientists, found that by focusing on gene changes caused by influences other than DNA sequences — called epigenetics — it was possible to reverse memory decline in an animal model of Alzheimer’s.

“We have not only identified the epigenetic factors that contribute to the memory loss, but we also found ways to temporarily reverse them in an animal model of Alzheimer’s,” said Zhen Yan, Professor at University at Buffalo in the US.

The research, published in the journal Brain, was conducted on mouse models carrying gene mutations for familial Alzheimer’s — where more than one member of a family has the disease — and on post-mortem brain tissues from Alzheimer’s patients.

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Poor sleep can predict Alzheimer’s Risk in elderly. Pixabay

Alzheimer’s is caused from both genetic and environmental risk factors, such as ageing, which combine to result in epigenetic changes, leading to gene expression changes, but little is known about how that occurs.

The epigenetic changes in Alzheimer’s happen primarily in the later stages, when patients are unable to retain recently learned information and exhibit the most dramatic cognitive decline, Yan said.

A key reason for the cognitive decline is the loss of glutamate receptors, which are critical to learning and short-term memory.

The researchers found that the loss of glutamate receptors is the result of an epigenetic process known as repressive histone modification, which is elevated in Alzheimer’s.

“Our study not only reveals the correlation between epigenetic changes and Alzheimer’s, we also found we can correct the cognitive dysfunction by targeting the epigenetic enzymes to restore glutamate receptors,” Yan said.

A lady suffering from Alzheimer’s. Flickr

The Alzheimer’s animals were injected three times with compounds designed to inhibit the enzyme that controls repressive histone modification.

In animals who received the enzyme inhibitor the cognitive function restored and was confirmed through evaluations of recognition memory, spatial memory and working memory.

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The improvements lasted for one week. Future studies will focus on developing compounds that penetrate the brain more effectively and are thus longer-lasting, the researchers said. (IANS)

Next Story

This Protein in the Human Brain Can Protect Against Alzheimer’s disease

Brain protein that could protect against Alzheimer's disease

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Immune cells in the brain, called microglia, play a critical role in Alzheimer's disease. Pixabay

Researchers have found that a protein that regulates white blood cells in the human brain could protect against Alzheimer’s disease.

The results published in the journal Communications Biology suggest that this protein, called CD33, could have important implications in the fight against Alzheimer’s disease.

“Immune cells in the brain, called microglia, play a critical role in Alzheimer’s disease,” explained study co-author Matthew Macauley, Assistant Professor at University of Alberta in Edmonton, Canada.

“They can be harmful or protective. Swaying microglia from a harmful to protective state could be the key to treating the disease,” Macauley added.

Scientists have identified the CD33 protein as a factor that may decrease a person’s likelihood of Alzheimer’s disease.

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CD33 protein in the brain plays a crucial role in modulating the function of microglia. Pixabay

Now, Macauley’s research has shown that the most common type of CD33 protein plays a crucial role in modulating the function of microglia.

“The fact that CD33 is found on microglia suggests that immune cells can protect the brain from Alzheimer’s disease under the right circumstances,” said Abhishek Bhattacherjee, first author and postdoctoral fellow in the Macauley lab.

Alzheimer’s disease affects more than 44 million people around the world.

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“These findings set the stage for future testing of a causal relationship between CD33 and Alzheimer’s Disease, as well as testing therapeutic strategies to sway microglia from harmful to protecting against the disease – by targeting CD33,” said Macauley.

“Microglia have the potential to ‘clean up’ the neurodegenerative plaques, through a process called phagocytosis — so a therapy to harness this ability to slow down or reverse Alzheimer’s disease can be envisioned,” Macauley said. (IANS)