Three more stories from the annual Movement Disorder Society meeting that was held in Sydney, Australia.
Researchers from Lund University in Lund, Sweden and the Van Andel Research Institute in Grand Rapids, Michigan, have developed a potentially useful new mouse model for studying Parkinson’s disease.
The accumulation of α-synuclein is one of the hallmarks of the development of Parkinson’s disease. If scientists can recreate this process in a mouse model, it will go a long way toward furthering their understanding of the cause of Parkinson’s. While some mouse models demonstrate certain particular pathologies of PD, they do have limitations. One such limitation is in demonstrating the progressive development that duplicates the slow accumulation of α-synuclein and loss of motor and non-motor symptoms as it happens in humans. This team of researchers has developed a new transgenic mouse model that parallels the slow age dependent accumulation of α-synuclein and demonstrates the behavioral deficits seen in humans. Understanding how α-synuclein increases in the brains of mice gives research a new tool to study how to treat it in humans and to better understand the causes of PD.
It has been suspected for some time that people with Parkinson’s develop malignant skin cancers more often than the general population. A study done through the University of Rochester demonstrated that Parkinson’s does bring a four fold greater risk. A new clinical trial followed 1700 newly diagnosed Parkinson subjects and researchers estimated that in this population there should be about just under four cases of malignant melanoma. In fact, they found 13 cases of new malignant melanoma. Why this is so is not yet understood. These findings prompted Matthew Stern, M.D. the Movement Disorder Society President-elect to say “This study underscores the importance for dermatologic screening in PD patients. Further, elucidating the relationship between PD and melanoma may shed light on the pathogenesis of both disorder.”
Reducing cognitive impairment in Parkinson’s is the goal of another study out of Newcastle University in Great Britain. They tested the effects of the drug apomorphine that has been used for over 20 years in Europe to reduce motor fluctuations in advanced PD. α-Synuclein accumulations are one known cause of dementia in PD, but amyloid -beta (Aβ) accumulations also contribute to dementia. This study looked at the brain tissue samples from both cognitively impaired and not impaired deceased Parkinson’s patients. They found that brain tissues of people treated with apomorphine for motor complications while living and found lower levels of Aβ. These findings suggest that apomorphine treatment may have significantly lowered the Aβ burden in the brains of non cognitively impaired individuals and alsomay have reduced the cognitive impairment in the cases of noted dementia.
Researchers stressed that this is an on-going investigation, but that it may be able to lead to a therapeutic treatment for dementia in PD and eventually lead to clinical trials.