Researchers at UCR(University of California, Riverside) may have found the cause of Alzheimer’s disease at the molecular level by looking deeper into the DNA structures in the brain of patients with dementia.

The researchers indicate that the important factor to understanding Alzheimer’s disease may lie in the “tau” proteins that form threads that eventually join to form tangles inside neurons. 

These tangles block the neuron’s transport system, which harms the synaptic communication between neurons.

Alzheimer's Disease
Image: Getty Images

Studies suggest that Alzheimer’s-related brain changes may result from a complex interplay among abnormal tau and a protein called beta-amyloid protein and several other factors. 

It appears that abnormal tau accumulates in specific brain regions involved in memory. 

Beta-amyloid clumps into plaques between neurons. 

As the level of beta-amyloid reaches a tipping point, there is a rapid spread of tau throughout the brain.

By studying more about the Combination of amyloid plaques and neurofibrillary tangles in the brain, a potential diagnosis for Alzheimer’s may arise.


Those plaques are the potential build-up of amyloid peptides in the brain and neurofibrillary tangles are made up of tau protein.

A little while back, UCR Chemistry Professor Ryan Julian and his colleagues studied the aspects of tau protein.

They analyzed this tau protein closely by hoping that this protein could unveil the reason behind amyloid plaques and neurofibrillary tangles.

By the time of inspection, they discovered an ambiguous difference in the form of tau. 

This helped the scientists to differentiate between people who did not express the sign of dementia and those who did. 

“Roughly 20% of people have the plaques, but no signs of dementia, This makes it seem as though the plaques themselves are not the cause,” 

says Ryan Julian, UCR Chemistry Professor.

“An isomer is the same molecule with a different three-dimensional orientation than the original,” Julian said. 

“A common example would be hands. Hands are isomers of each other, mirror images but not exact copies. Isomers can actually have a handedness.”, he added.

Usually, proteins in living organisms are made from left-handed amino acids. But those who have a build-up of dementia, plaques or tangles show a different-handed form of amino acid.

Julian said, 

“If you try to put a right-handed glove on your left hand, it doesn’t work too well. It’s a similar problem in biology; molecules don’t work the way they’re supposed to after a while because a left-handed glove can actually convert into a right-handed glove that doesn’t fit,”

The process of diminishing defective proteins from cells, known as Autophagy slows down in people over the age of 65.

It isn’t clear why this is happening yet, but Julian’s team is planning to study more about this.

Several studies have shown autophagy deficits may occur in the early stage of Alzheimer’s disease. 

Autophagy itself plays an important role in the generation and metabolism of amyloid proteins, assembling of tau, and its dysfunction may lead to the progress or aggravation of Alzheimer’s disease.

Some drugs are effective in prompting autophagy and some aren’t. Studies say autophagy can be activated by fasting and proper dieting. 

Taking these measures, combined with drug therapies, may ultimately help prevent the disease.


Julian said,

“If a slowdown in autophagy is the underlying cause, things that increase it should have the benefit, opposite effect,” 

By observing this microscopic cause of potential build-up of dementia, researchers are giving hope to humanity that we may say goodbye to Alzheimer’s disease.

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