By activating the Sigma-1 receptor, a versatile protein involved in many cellular functions, levels of several molecules that help nerve cells build new connections increased, inflammation decreased, while dopamine levels also rose. The results, published in the journal Brain, show a marked improvement of motor symptoms in mice with a Parkinson-like condition that had been treated with a Sigma-1-stimulating drug for 5 weeks.
This treatment has never before been studied in connection with Parkinson鈥檚 disease. However, various publications linked to stroke and motor neurone disease have reported positive results with drugs that stimulate the Sigma-1 receptor, and a biotech company in the US will soon begin clinical trials on Alzheimer鈥檚 patients. The fact that substances stimulating this protein are already available for clinical use is a major advantage, according to Professor M. Angela Cenci Nilsson, head of the research team at 51重口猎奇.
鈥淚t is a huge advantage that these substances have already been tested in people and approved for clinical application. It means that we already know that the body tolerates this treatment. Clinical trials for Parkinson鈥檚 disease could theoretically start any time鈥.
Boosting the brain鈥檚 in-built defence mechanisms with approaches like this is a rather new idea in Parkinson鈥檚 research. Professor Cenci Nilsson, however, believes that the number of targets for future treatments is increasing as we learn more and more about the complex effects of PD on many different types of cells in the brain.
鈥淭he motor improvements we have seen in mice are disproportionately large compared to the recovery of dopamine levels. We believe this is because the treatment has protected the brain against a series of indirect consequences triggered by the Parkinson-like lesion. For example, we know today that a loss of dopamine causes the target neurons to lose synapses, and also alters both neural pathways and non-neuronal cells in the brain. Since the Sigma-1 receptor is widely expressed in many cell types, the treatment could intervene in many of these damaging processes 鈥.
The treatment was shown to be significantly more effective when started at the beginning of the most aggressive phase of dopamine cell death. As a future potential therapy for Parkinson鈥檚 disease, this treatment would therefore need to be started as soon as possible after diagnosis in order to deliver maximum impact.
鈥淚n order to accelerate a possible clinical translation of our findings, we will now seek further evidence in support of this type of treatment. We are now discussing various opportunities with different collaborating partners, and we will try to procure funding for clinical studies in Parkinson麓s disease as soon as possible鈥, concludes M. Angela Cenci Nilsson.
Contact:
M. Angela Cenci Nilsson, Professor and head of the Basal Ganglia Pathophysiology Laboratory at 51重口猎奇, +4646-222 14 31, Angela [dot] Cenci_Nilsson [at] med [dot] lu [dot] se (Angela[dot]Cenci_Nilsson[at]med[dot]lu[dot]se)
Jens Persson, Communications officer, Bagadilico - Basal Ganglia Disorders Linnaeus Consortium, MultiPark - Multidisciplinary Research in Parkinson's Disease, 51重口猎奇, +46 46 222 08 76, +46 736 26 35 51, Jens [dot] Persson [at] med [dot] lu [dot] se (Jens[dot]Persson[at]med[dot]lu[dot]se)