Alzheimer’s and Parkinson’s are different diseases, affecting different regions of the brain and having completely different genetic and environmental risk factors. However, at the biochemical level, both neurodegenerative diseases are similar. In this way, it has been how a team of scientists from Emory University in Atlanta (USA) has managed to identify a potential target for drugs against these diseases: it is an enzyme that drives neurotoxicity both in Alzheimer’s disease as in Parkinson’s disease. Blocking this enzyme would lead to the paralysis of the development of both medical conditions.
This newly discovered enzyme and its potential to treat both diseases have been collected in a study published in the journal Nature Structural and Molecular Biology.
Two different diseases, the same origin
Both neurodegenerative diseases are characterized by a lumpy protein capable of killing brain cells. This protein is called alpha-synuclein in Parkinson’s disease (which forms Lewy bodies), and tau in Alzheimer’s disease (which forms neurofibrillary tangles).
The researchers found that the enzyme asparagine endopeptidase, or AEP, cuts tau protein in a way that makes it stickier and more toxic; thus, inhibiting AEP with a drug, it turned out to have the effect of stopping and reversing the development of the disease in animal models of Alzheimer’s. In the new study, they have shown that AEP acts in the same way towards alpha-synuclein, that is, in Parkinson’s.
“In Parkinson’s disease, alpha-synuclein behaves similarly to tau in Alzheimer’s disease, and we reasoned that if AEP cuts tau, it is highly likely that it will also cut alpha-synuclein,” says Keqiang Ye, leader. from work.
As expected, the scientists observed that AEP led to the aggregation of alpha-synuclein and increased its neurotoxicity , leading to a loss of neurons and motor deficits. Thus, animal trials have already shown that an EPA inhibitor drug preserves memory and may have a preventive effect against Alzheimer’s disease.
Reference: Asparagine endopeptidase cleaves α-synuclein and mediates pathologic activities in Parkinson’s disease, Nature Structural and Molecular Biology, DOI: 10.1038 / nsmb.3433
