Alzheimer's disease is transmitted from the neuron to the neuron
Last reviewed: 23.04.2024
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Scientists from the Van Andel Research Institute (VARI) and the University of Lund (Lund University), Sweden, published a study specifying the mechanism of spreading the brain of Parkinson's disease. Experiments on rats with a model of this neurodegenerative disease reveal a process that previously explained mad cow disease: the migration of misfolded proteins from patients to healthy cells. This model has never before been so clearly demonstrated on a living body, and a breakthrough by scientists makes us a step closer to drugs that are able to actively intervene during Parkinson's disease.
"Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's," says study leader Patrik Brundin, MD, PhD. "The main unsatisfied medical need is a method of treatment that slows the progression of the disease. We are striving to better understand how Parkinson's disease progresses, and thereby find new molecular targets for drugs that can change the course of the disease. "
Previous studies have shown that in young healthy neurons transplanted into the brain of patients with Parkinson's disease, an incorrectly folded protein, known as alpha-sinuclein, gradually appears. This discovery was a prerequisite for the hypothesis put forward by Dr. Brundin's group on the transfer of protein from the cell to the cell, which was subsequently demonstrated in laboratory experiments.
In a study published in the Journal of the Public Library of Science One, scientists for the first time were able to track events in the recipient cell during the absorption of a pathological protein passing through the outer cell membrane. In addition, experiments have shown that the absorbed alpha-synuclein attracts host cell proteins, inducing an abnormal intracellular folding or aggregation. "This cellular process probably leads to a pathological process of progression of Parkinson's disease, and as the patient worsens, it spreads to an increasing number of brain regions," suggests lead author of the study Elodie Angot, PhD.
"In our experiments, we showed the nucleus of a pathological human alpha-synuclein protein surrounded by alpha-synuclein synthesized by the rat itself. This means that an incorrectly folded protein not only moves between cells, but also acts as a "grain", attracting proteins produced by rat brain cells, "says another lead author of the study, Jennifer Steiner, PhD.
Nevertheless, it remains unclear how exactly alpha-synuclein obtains access from the extracellular space into the cytoplasm of the cell, becoming, in turn, a template for the wrong folding of the naturally existing alpha-synuclein. To clarify this important stage of the process, further research is needed.
This finding does not disclose the root causes of Parkinson's disease, but in combination with disease models developed at both Lund University and other research centers, it can help find new targets for medications that can alleviate symptoms or slow the progression of the disease, affecting today more than 1 % of the population over the age of 65.
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