Scientists discover the possible cause of Alzheimer’s disease!

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The origin of Alzheimer’s disease has baffled scientists for more than a century, but new research claims to have discovered the culprit – it may be caused by a slowing of the ability of cells to clean themselves.

Researchers from the University of California, Riverside (UCR), suggest that the slowdown is observed in people over 65 – the appropriate age for diagnosis – and is a possible cause of unhealthy accumulation in the brain.

The slowdown, known as autophagy, can be caused by fasting, in which cells do not get enough protein from an individual’s diet – and they fill in the void by recycling proteins already in the cells.

Drugs are already being tested to improve autophagy, and if this is the cause of Alzheimer’s disease, we could see a potential preventative drug in the near future, says Ryan Julian, a professor of chemistry at the University of California, Los Angeles, who led the study.

“If slowing down in autophagy is the root cause, things that increase it should have a beneficial and opposite effect,” Julian said.

The disease was discovered by Dr. Alius Alzheimer in 1906, who observed changes in the brain tissue of a woman who died of unusual mental illness – and how it occurs since then has remained a mystery.

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Doctors usually diagnose Alzheimer’s disease when they find a mixture of amyloid plaques and neurofibrillary tangles, along with the dimensions.

However, Julian said in a statement: “Approximately 20% of people have plaques, but there are no signs of dementia. This makes it appear as if the plaques themselves are not the cause.”

Now, Julian and his colleagues think they have deciphered the disease by looking at proteins inside the brain.

The abnormal buildup is known to cause Alzheimer’s disease, which includes two types of proteins: one called amyloid, whose deposits form plaques around brain cells, and another called tau, which forms tangles inside brain cells.

The team began the study by focusing on tau proteins, which have been found to be abnormally malformed in the brains of people with Alzheimer’s disease.

Tau proteins help stabilize the internal skeleton of nerve cells, also known as neurons, in the brain.

Although difficult to detect, the different form of the tau allowed scientists to distinguish people who did not express any outward signs of dementia from those who did.

Julian’s lab at the university is focusing on the different forms a single molecule can take, called isomers, which also helped point them to the culprit.

“The isomer is the same molecule with a different 3D orientation than the original,” Julian said.

The team examined all of the proteins in the donated brain samples. Those with brain buildup but not dementia had normal tau, while a different form of tau was found in those who developed plaques or tangles as well as dementia. Most proteins in the body have a half-life of less than 48 hours, but if they are found to remain, some amino acids can be converted to another isomer.

Source: Daily Mail



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