The discovery is sure to pave the way to better treatments for Alzheimer's disease, which, despite the progress made within the last five years, still suffers from a truly effective therapy to halt or reverse the advancement of the disease.
Scientists, from The Johns Hopkins University School of Medicine, discovered that chemicals called prostaglandins, can protect the cells from amyloid â-peptide 42 (Aâ1-42), the compound related to the onset of Alzheimer's.
Prostaglandin E2 (PGE2) is produced via the action of the COX-2 enzyme, which can contribute to brain injury.
In spite of the negative effects of COX-2, ongoing studies have shown that PGE2 can actually provide some protection against brain cell death by binding to various PGE2 receptors.
In the study, published in the European Journal of Neuroscience, co-lead researcher Sylvain Doré, an associate professor of anesthesiology and critical care medicine and neuroscience, and researchers focused on four specific PGE2 receptors, EP1-4, in cortical neuronal cells cultured from postnatal mice.
Because neuroinflammation is thought to play a role in the development of AD, PGE2 was a logical place to look for clues to AD toxicity and brain cell death, according to Doré.
Although it's known that PGE2 can offer protection against neurotoxicity, Doré's study shows the protection is linked to stimulation of receptors EP2 and EP4.
This stimulation results in a cascade of events inside brain cells that produces cyclic-AMP (cAMP), a molecule that protects brain cells by reducing the toxic effects of Aâ1-42.
Doré theorised the presence of Aâ1-42 in neuritic plaque, a waxy translucent substance and a hallmark in the brains of AD patients, may cause cellular death by self-assembling into long protein filaments that are toxic to neurons.
It's also possible, Doré said, that prostaglandin protection works by modifying the link between Aâ1-42 and the overproduction of free radicals. Free radicals have been linked with neuronal loss observed in AD.
"The development and testing of molecules that can enhance PGE2 receptor activity, and further research into how these receptors increase cAMP concentrations and improve protection could lead to successful new treatments," Doré said.
"Due to the established link between Aâ1-42 and Alzheimer's disease, this discovery could lead to better drug therapies for treating this disease," he added.
Current therapies, the most effective being Cholinesterase Inhibitors, delay the break down of acetylcholine in the brain. Acetylcholine helps communication between the nerve cells and is important for memory.
Donepezil (Aricept), rivastigmine (Exelon), and Razadyne (galantamine HBr) are most effective in the early stages of Alzheimer's disease.
This group of prescription drugs has been shown to have some modest effect in slowing the degeneration of cognitive symptoms.
The drugs can also reduce the behavioral problems that are exhibited in people with Alzheimer's.
When the drugs work well they can significantly improve people's quality of life. Benefits, if they occur, should happen within a few weeks.