Alzeimer’s disease reversal on the cards?

Researchers have identified an enzyme that could halt or possibly even reverse the build-up of toxic protein fragments known as plaques in the brains of mice with Alzheimer’s disease. Plaques decre

By: Admin | | Updated: February 26, 2014 11:52 am

Researchers have identified an enzyme that could halt or possibly even reverse the build-up of toxic protein fragments known as plaques in the brains of mice with Alzheimer’s disease. Plaques decreased substantially in mice treated with gene therapy to increase activity of the enzyme neuraminidase 1 (NEU1) in a region of the brain involved in learning and memory. NEU1 belongs to a family of enzymes in cells whose job is to dismantle and recycle unneeded proteins and other components. The enzyme is missing or reduced in a rare inherited disorder called sialidosis that can affect children and adolescents. Also Read - Demi Lovato suffered three strokes and a heart attack; Here’s everything you need to know

The work was done in a mouse lacking the NEU1 gene developed in laboratory of study’s corresponding author Alessandra d’Azzo, Ph.D., a member in the St. Jude Department of Genetics. The study revealed that loss of NEU1 activity was linked with a build-up in lysosomes of the amyloid precursor protein (APP) that they identified as a natural target of the enzyme. Improperly processed, APP is broken into the toxic peptides that form Alzheimer’s plaques. Those fragments include amyloid beta peptide 42 (A beta-42), which researchers suspect play a major role in the Alzheimer’s disease process. Also Read - Attention night owls! Staying up late night can make you more prone to depression

Not only did APP accumulate in lysosomes of mice lacking NEU1 but researchers found evidence that the build-up promoted the production of A beta-42 and other toxic peptides tied to Alzheimer’s disease.
A beta-42 was detected in the spinal fluid and hippocampus of mice that lacked NEU1, but not in mice with a functional NEU1 gene. Also Read - Aggressive and bullying behaviour: Is ‘Bigg Boss 14’ injurious to your mental health?

Loss of NEU1 also accelerated the disease process in mice bred to mimic early-onset Alzheimer’s in humans. Without the enzyme, both APP and the protein fragments that make up plaques accumulated faster in these mice.

But within weeks of using gene therapy to bolster NEU1 activity, d’Azzo’s group reported that plaques declined dramatically in the hippocampus of treated mice.

The research has been published in the journal Nature Communications.

What is Alzheimer’s?

Alzheimer’s is a kind of dementia that causes problems with memory, thinking and behaviour. It is found in close to 80% of those suffering from dementia and is therefore the most common type. It is commonly believed that Alzheimer’s is a condition that strikes only the elderly, but this is not necessarily true. While the chances of developing the disease increase with age, it is now seen that younger people are also now being diagnosed with the disease.

One of the first signs of Alzheimer’s is memory loss. It is usually a gradual process and gets ignored in a number of cases. This is followed by a decrease in other aspects of cognition such as word-finding, vision/spatial issues and impaired reasoning or judgement. As the disease progresses, newer symptoms start showing. The patient suffers damage in areas of the brain that control language, reasoning, sensory processing, and conscious thought. Memory loss and confusion become worse, and the person begins to have problems recognizing family and friends. People with Alzheimer’s find it exceptionally difficult to learn new things, carry out tasks that involve multiple steps (like getting dressed) and cope with new situations. They may have hallucinations, delusions, paranoia, and may behave impulsively. As they progress to the more severe stages of Alzheimer’s disease, the brain completely shrinks and the patient becomes increasingly dependent on others. Read more…

With inputs from ANI

Published : December 4, 2013 2:19 pm | Updated:February 26, 2014 11:52 am

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