Development of the Parkinson disease.
Parkinson's disease (PD) is the second most frequent neurodegenerative disease, after Alzheimer; about 1% of 55+ years old and 3% of 70+ years old have the disease. In a small minority of PD patients (5-10%) a hereditary form is diagnosed, whereas in the vast majority (so-called sporadic PD) the cause is unknown. PD is pathologically characterized by the death of dopamine producing neurons in a specific part of the brain. A second pathological characteristic are the presence of aggregates of misfolded proteins in the brain. The average age at which patients start to display clinical motoric symptoms, such as tremors (hyperkinesia) or rigidity (hypokinesia) is around 60, characterizing PD as a typical ageing-related disease. However, before motoric symptoms develop, pre-motoric symptoms are typically observed, such as sleep disturbance, obstipation, depression and types of dementia.
The current medication, with dopamine replacement therapy for example, primarily aims at suppression of disease symptoms, not on stopping of repair of the underlying pathology.
BPRC has a well-characterized experimental model of sporadic PD in a non-human primate, the common marmoset. PD is induced by injection of MPTP, a non-toxic substance which is converted into the toxic metabolite MMP+ that is selectively taken up in dopaminergic neurons and inhibits the cell's respiration. Marmosets injected with MPTP develop characteristic premotoric (sleep disturbance) and motoric symptoms (both hyper- and hypokinesia).
Research in the model by BPRC is focused:
- the development of quantifiable detection methods for pre-motoric and motoric symptoms,
- a better understanding of the processes contributing to the pathology and clinical expression of PD,
- the development of pharmaceutical and non-pharmaceutical therapies aiming at stopping the neurodegenerative process, promote repair, suppress disease symptoms and preventing side effects of the current medications.