How Alzheimer’s protein breaches cell membranes


New York — New research led by an Indian-origin scientist has found how protein that collects in the brain of persons with Alzheimer’s disease penetrates the cell membranes.

The findings, published in the Journal of Biological Chemistry, could lead to novel therapies for age-related diseases.

The protein amyloid-beta builds up in the brains of persons with Alzheimer’s disease, ultimately aggregating into sticky clumps called plaque on the surface of neurons.

“From our study it is clear that the cell membrane is the hot spot where amyloid-beta becomes crazy,” said Ayyalusamy Ramamoorthy, Professor at University of Michigan in the US.

The researchers found that thinner parts of the neuronal membranes give access points to amyloid-beta, allowing the protein to puncture and kill those cells, and destroying the patient’s ability to make and retain memory.

These thin spots are composed of short fatty acid chains whereas the thicker parts of the membrane are composed of long fatty acid chains.

The formation of lipids with short chains — caused by ageing or other physiological means that result in Alzheimer’s — can promote cell death from the accumulation of amyloid-beta, according to the researchers.

“We’re trying to understand how components of the cell membrane and the physical and chemical properties of the lipid membrane would influence the aggregation of amyloid-beta by a variety of biophysical techniques,” Ramamoorthy said.

“The thickness of cell membranes is very important not only for Alzheimer’s disease, but also for diabetes and other aging-related diseases,” Ramamoorthy noted.

Currently, Ramamoorthy’s team is screening libraries of small molecular compounds that could target the aggregation of amyloid-beta within a person’s cell membrane.

“These findings could be significant in the potential development of compounds to treat the aging-related diseases,” he said.


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