SFB-F44 - Cell signaling in chronic CNS disorders

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Parkinson's disease

Parkinson’s disease

Parkinson's disease (PD) is a complex neurodegenerative disorder of the central nervous system and is the most common neurodegenerative disorder. It is commonly accepted that 1-2 % of the population older than 60-65 years are affected by PD. Worldwide currently more than 4 million PD patients have been diagnosed. In Austria the number of PD patients is 20,000. Men are often more affected than women: In most studies the male-to-female ratio is about 3:2. The mean age of disease onset is 64.1 years, although PD occurs infrequently in 5–10% of patients aged between 20 and 50 years. A juvenile PD onset also exists (before age 20).

Due to a spreading process of α-synuclein aggregation and neuronal loss, starting in the olfactory tract as well as lower brainstem and ultimately involving cortical areas, PD comes along with motor and non-motor symptoms. Motor impairment is characterised by bradykinesia (slowness of movement with a progressive loss of muscle control), rest tremor (also called parkinsonian tremor), rigidity (increased muscle tone and passive movement) and postural instability or impaired balance – all together universally known as parkinsonism. Non-motor symptoms include depression, hyposmia, REM sleep behaviour disorder, constipation, urinary incontinence and postural dizziness. The cause of PD is unknown, which is the reason why nothing can be done to stop the progression of the disease. Presumably complex interaction between genetic and environmental factors may play a role. A small number of individuals are at increased risk because of their family history. Various risk factors have been found for spontaneous PD, but how far they relate to the pathogenesis is still not known.

Generally human brain cells of the midbrain produce one of the most important neurotransmitters: dopamine, which is responsible for a smooth movement of muscles among other functions. PD results from the death or degeneration of these dopamine-containing cells. That will lead to impaired activation of cortical motor programs, resulting in slowness of movements. During the advanced stage of PD, cognitive and behavioural problems arise, as well as sleep disturbances, emotional problems and dementia.

Diagnosis and modern treatments are mainly based on PD symptoms, but PD can be confused with many disorders. Therefore only clinical experience guarantees diagnostic precision. Most therapeutic strategies are designed to increase the level of dopamine in the human brain, mainly by using levodopa and dopamine agonists. Diet and some forms of rehabilitation have shown some effectiveness at relieving symptoms. For some  PD patients, surgery and deep brain stimulation may be an option to reduce motor symptoms when drugs are ineffective. In the last decades, considerable progress has been made in the field of experimental studies, genetics and pathophysiology and there have been major endeavours to understand the pathomechanism of PD, but none of them have been translated into neuroprotective therapies in people. A major pharmacotherapeutic goal is therefore to discover new signaling pathways that can be modulated by drugs to protect the dopamine neurons from degeneration and thereby slow (or even prevent) the development of the disease. One such pathway is also currently being studied within our research network.

Further reading