Alzheimer's: Scientists find possible new target for early treatment

Evan Walker
Evan Walker TheMediTary.Com |
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Scientists may have found a target for new treatments for Alzheimer’s disease. Pansfun Images/Stocksy
  • With an aging population worldwide, neurodegenerative diseases, such as dementia, are an increasing problem.
  • Although there are treatments for neurodegenerative diseases, these generally alleviate symptoms, rather than changing the course of the disease.
  • Now, research has found that a protein that regulates cell repair could be a promising new target for treating several of these conditions, including the most common, Alzheimer’s disease.

Neurodegenerative diseases occur when nerve cells in the brain and peripheral nervous system lose function and eventually die. They include Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS — also known as motor neuron disease), among others.

In the United States, an estimated 6.9 million people aged 65 and over are living with Alzheimer’s disease, and around a million have Parkinson’s. ALS is less common; the CDC estimates that around 31,000 people in the U.S. have the condition.

Current treatments can alleviate symptoms and some slow the progression of the diseases, but no cures are yet available. New monoclonal antibody treatments for Alzheimer’s have shown some potential for modifying the course of the disease, but many experts are concerned about side effects.

In the search for new therapies, research from Penn State University has identified a group of proteins that could be a target for new treatments for Alzheimer’s and other neurodegenerative disorders.

The researchers, who have a patent related to this work, found that reducing the function of heparan-sulfate-modified proteoglycans (HSPGs) helped reverse cell damage from neurodegenerative diseases.

Their study is published iniScience.

“This is interesting research which shows how cells might be protected from the effects of genetic mutations that cause Alzheimer’s disease. However, as it has only been shown in fruit flies and human cells from outside of the brain, it’s hard to say just how relevant the findings are at the moment. We’re excited to see the next stage of this research, to see if similar effects can be seen in human brain cells.”

— Katherine Gray, Alzheimer’s Society’s head of research

To verify their findings, the researchers used an animal model of Alzheimer’s. They used fruit flies that had been modified to have deficits in presenilin protein, which mimics the effect of a mutation in the Health">presenilin gene, PSEN1, the most common cause of familial (early-onset) Alzheimer’s.

Selleck explained that a rare genetic change in another protein, APOE, can delay the effect of the PSEN1 mutation, sometimes for decades. He suggested that targeting these two substances and the enzymes that make heparan sulfate could help prevent neurodegeneration in people.

In the fruit flies, the researchers reduced the functioning of HSPGs, which suppressed the death of nerve cells and corrected other cell defects.

They suggest that disrupting the structure of heparan sulfate modifications blocks or reverses early cellular problems in these models of Alzheimer’s.

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