What are the causes of Parkinson's memory gaps?

What are the causes of Parkinson's memory gaps?

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Researchers discovered mechanism that leads to memory deficits in Parkinson's

Parkinson's is not only characterized by motor disorders, but also by memory impairment, although it remains largely unclear how the latter develop. Scientists at the University Medical Center Göttingen and researchers at the Instituto de Medicina Molecular (Lisbon) have now found out which molecular process is responsible for the loss of memory in Parkinson's. This also opens up new approaches for the treatment of the disease.

According to the scientists, the gaps in memory in Parkinson's disease are triggered by a protein interaction, which leads to disorders in communication between the nerve cells. However, the effect can be remedied by "genetic manipulation and the use of antibodies" and the memory can be restored. The newly discovered molecular signaling pathway could thus be used as a starting point for the treatment of cognitive impairments in Parkinson's. The study was published in the specialist journal "Nature Neuroscience".

Molecular pathway identified

Typical motor symptoms in Parkinson's are the so-called tremor (trembling of the limbs), a stooped posture, difficulty walking and a severely restricted facial expression. Added to this are "deficits in memory during the course of the disease"; explain the scientists. So far, however, relatively little was known about the origin of these cognitive side effects. In experiments on mice, the researchers from Göttingen and Lisbon have now for the first time shown in detail a molecular signaling pathway that leads to the development of cognitive deficits that are similar to those in Parkinson's patients.

Fatal interaction between proteins

According to the researchers, the newly discovered signaling pathway is activated by the interaction of abnormal forms of the alpha-synuclein protein with the prion protein (PrPC). PrPC was already known to be involved in processes that lead to age-related behavioral abnormalities and impaired memory in neurodegeneration, according to the Göttingen University Medical Center. The scientists were able to show that the interaction between alpha-Synuklein and PrPC triggers a cascade of processes that ultimately lead to disturbances in the contacts between nerve cells (synapses). This affects the communication of the affected nerve cells and promotes the development of cognitive deficits.

Parkinson's is much more than a motor disorder

"We now know that Parkinson's disease is much more than a motor disorder"; emphasizes study coordinator Professor Dr. Tiago Outeiro, Director of the Department for Experimental Neurodegeneration at the University Medical Center Göttingen. It was already known that certain forms of the alpha-synuclein protein can cause malfunctions in the communication of nerve cells that are responsible for memory, the expert continues. However, it has so far remained unclear exactly how this is done. “Now we know more about the molecular mechanisms. This opens up new therapeutic approaches for the prevention and treatment of Parkinson's disease, ”said Prof. Tiago.

New approaches to therapy

In their study, the scientists describe for the first time a new “mechanism that is sufficient to initiate early damage to the synapses of nerve cells that is caused solely by extracellular alpha-synuclein,” reports the University Medical Center Göttingen. The interaction of the proteins sets in motion a signal cascade that leads to an incorrect regulation of the calcium balance and a malfunction of the synapses of nerve cells in the brain. If the protein is inactivated by genetic manipulation or the use of antibodies, the toxic effects of the alpha-synuclein oligomers are eliminated, the scientists explain. "In a mouse model for Parkinson's, there are no synaptic and cognitive deficits if this signal path is blocked," emphasize Prof. Tiago and colleagues. This opens up completely new approaches for Parkinson's therapy. (fp)

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Video: Parkinsons disease - a journey through a brain (August 2022).