Parkinson’s disease: “The brake” can lift the cell death in some patients

A new treatment for a type of Parkinson disease can be on the horizon after researchers discovered a “bra” that can lower the death of the cell.

The study, carried by the warrants from Stanford University, California, involves a form of neuroodic disorder that is caused by a single genetic mutation.

This motion causes an excess of a protein that interferes with the ability of the cerep to protect. Inhibit of this protein, the found team, can stop the damage and allow to die of neurons to die for recovering.

“These discoveries suggest that it could be improved, the patient’s condition,” said card disease and stanford key, however it is “if patients can be identified fairly”, added.

While the most recognized synthes of Parkinson could rest tremors, the first signs of the disease also expresses some 15 years before.

These first signs, pffer said, include a steady-loss of smell and the disorder of sleep behavior, a condition in which people act their dreams.

In the United States, estimated that some 1.1 million people are living with Parkinson’s disease – a figure just expected to rise in the nearby Foundation of the Park.

As pkffer and their colleagues explain, around a quarter of all of the genetic motion, with one more in the most in repetitive lekine kinase 2 (lrrrk2).

Too LRRK2 in the brain changes cell structure that causing her “antenna” (technically the primary cilia) allowing you to send chemical messages.

In a healthy brain, communications are delivered back and forth between dopamine neurons in two regions of the brain known as the nigra noun.

When the Neurons of Dopamine are stressed, they call it-based sign in the stratum called sounds of sounds of course they relocate other celles.

When the lrrk2 activity crosses a certain threshold, the loss of primary cilia in stritum’s cells from receiving the hedgeog sonic sign; As a result, neuroproptive factors are not produced.

“Many kinds necessary for cells to survive are regulated across and receiving signs” “explain the explanatory explained.

“The cells in the strike that the factors of neuroproptive secrets in response to Hedgehog signals need Hedgehog to survive.

“Let’s think that when the celia lost their bilia, circus to death for death because they need to get bilia you keep mixed.”

It is possible to fight lrRk2 using a “Mli-2 lRRK2 Kinase inhibitor,” a molecule that attaches to the enzyme and reduce their business.

In their study, petters and graders off I am to try if I could still neurons too.

At first, the results were not prompting. The team has given the inhibitor for two weeks to the mice that has had the lrrl2 mutation (and showing consistent symptoms with Parkinson Park disease)

However, researchers were insulated for the recent entails cry to awake, that the Primiers returned to third party and one year.

“The results that non-division cells grow to understand that it is possible theoretical by the inibre of the work,” said PFEFFER.

Inspired by this, the team decided to try to give the mice the iniber for more time – with the results in three months because “sblanding.” The added biochemum.

The hardest treatment has seen the percentage of straratory neurons and throat with the primary cilia in thi with the mutation for the same level as a regular mice.

This had the effect of restoring the communication between Dopamine neurons and streaked, driving to the Normal Neurophotective factors.

The researchers also found that the level of hedgehog’s signs of the neurons of Depamine decreased-suggest they were under less stress.

In the support of density density dennity support in the stool of the quarry was found in the query of hours, suggestion that had been in the process of dying.

With its full initial study, researchers say their next step to determine if other forms of Parkinson that are not associated with the lrRk2 mutuation could also benefit from the new treatment.

This is possible, Pexffer explains, because the mutation is not the only way to end with a lrRK2 of lrRk2 for overcatative. In fact, added, the inhibitor treatment could also help with a neurophending disease.

“We’re very elence on these goals. They suggest this approach has a big promise to help patients in this neuronal circuit in this brain.

She has concluded: “There is multiple lrRk2 clinical programs invironed – and our hope is that these discoveries in the mice to be true for patients in the future.”

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Reference

Jaimon, e. Lin, yr., Tonels, f.icico, Аico, o., Alessi, dr, & p popffer, sr (2025). Restore of Neuroprotective Neuroprotective Striatrices from Parkinson Cice-Mutant Tice Iniber’s Treatment. Seghers of science, 18th(793).