They were Portuguese scientists who discovered, in a study with rats, the cellular mechanism that may explain the lack of memory in Parkinson’s patients.
This study was conducted by researchers from the Institute of Molecular Medicine (iMM), Lisbon, and the Nova universities of Lisbon and Göttingen, Germany. This revealed that a protein that accumulates in the brain of Parkinson’s patients, alpha-synuclein, interacts with another protein, PrP, which functions as a sensor, thus generating changes in the functions of neurons (brain cells) in turn linked the memory.
When administered a caffeine drug to rats with excess alpha-synuclein, the team of Luísa Lopes (iMM) and Tiago Outeiro (University of Göttingen and Center for Chronic Disease Studies of Universidade Nova de Lisboa) verified through tests of behavior, which memory deficits reverted.
“Animals were more likely to find clues” than those who were not treated with the drug, Imm researcher Luísa Lopes told Lusa.
Tiago Outeiro, said the drug works on another protein, adenosine A2A receptors, which mediate the interaction between alpha-synuclein proteins and PrP.
“If we inhibit A2A receptors, we avoid the toxic signal emitted by alpha-synuclein to PrP”, he said.
The next step of the work in development will be to characterize the interaction between alpha-synuclein and PrP proteins, to “design drugs” that block this interaction as well as its effects on memory and cognitive ability, test them on rats and monkeys.
Still, according to Tiago Outeiro, the therapies available for Parkinson’s disease only treat motor dysfunctions (tremors, difficulty walking, and stiff muscles are some of the symptoms). But as the disease progresses, memory and cognitive deficits and dementia arise.
All the results of this study were published in the journal Nature Neuroscience.