New York: Researchers have found that blocking a key receptor in brain cells could play a major role in diffusing the biological consequences of Alzheimer’s disease.
The human body's use of oxygen to produce energy often results in the formation of highly reactive molecules called oxygen free radicals.
Oxidative stress occurs when the production of these free radicals is greater than the body's ability to detoxify them.
The researchers discovered that the free radicals produced from oxidative stress actually bind to a protein receptor in the brain called the thromboxane receptor, or TP, and transmit signals to the neuronal cells to increase the production of amyloid beta or phosphorylated tau (tangles), the two major Alzheimer's pathologies.
"For the first time we have identified this receptor as the culprit responsible for the bad things that happen with the disease when high levels of oxygen free radicals are produced," said Domenico Pratico, professor of pharmacology, microbiology and immunology at the Temple University in the US.
The researchers introduced free radicals into the brain of a mouse model for Alzheimer's and witnessed a worsening of the animal's memory and learning capabilities, as well as an increase in amyloid beta and tangles.
However, they also treated a subset of the mice with a compound known to block the TP receptor in the brain.
In this group, said Pratica,, there was no manifestation of the cognitive impairment experienced by the non-treated mice.
The study appeared in the journal Neurobiology of Aging.