Parkinson’s disease is a progressive disease of the nervous system marked by tremor, muscular rigidity, and slow, imprecise movement, chiefly affecting middle-aged and elderly people. It is associated with degeneration of the basal ganglia of the brain and a deficiency of the neurotransmitter dopamine.
Nerve cells use a brain chemical called dopamine to help control muscle movement. With Parkinson’s disease, the brain cells located in the substantia nigra that make dopamine become impaired or die. Researchers do not know the cause of the death of the cells in the substantia nigra however. Without dopamine, the nerve cells that control movement is not able to send messages to the muscles. Researchers …show more content…
In Parkinson’s rigidity, the muscle tone of an affected limb is always stiff and does not relax, sometimes contributing to a decreased range of motion.
• Resting tremor – an uncontrollable movement that affects a limb when it is at rest and stops for the duration of a voluntary movement
• Postural instability – problems with standing or walking, or impaired balance and coordination
• Micrographia: This term is the name for a shrinkage in handwriting that progresses the more a person with Parkinson’s writes. This is a result of bradykinesia which causes difficulty of repetitive actions.
• Other physical symptoms, such as gait problems and reduced facial expression, may also occur due to the same disruption of movement that causes the better-known tremor and slowness
Most people with Parkinson’s experience nonmotor symptoms, those that do not involve movement, coordination, physical tasks or mobility.
• Cognitive impairment – decline in ability to multi-task and/or concentrate and potentially decline in intellectual functioning
• Mood disorders – depression and …show more content…
Clinically, this disease is characterized by bradykinesia, resting tremors, and rigidity due to loss of dopaminergic neurons within the substania nigra section of the ventral midbrain. In the normal state, release of the neurotransmitter dopamine in the presynaptic neuron results in signaling in the postsynaptic neuron through D1- and D2-type dopamine receptors. D1 receptors signal through G proteins to activate adenylate cyclase, causing cAMP formation and activation of PKA. D2-type receptors block this signaling by inhibiting adenylate cyclase. Parkinson’s disease can occur through both genetic mutation (familial) and exposure to environmental and neurotoxins (sporadic). Recessively inherited loss-of-function mutations in parkin, DJ-1, and PINK1 cause mitochondrial dysfunction and accumulation of reactive oxidative species (ROS), whereas dominantly inherited missense mutations in α-synuclein and LRRK2 may affect protein degradation pathways, leading to protein aggregation and accumulation of Lewy bodies. Mitochondrial dysfunction and protein aggregation in dopaminergic neurons may be responsible for their premature degeneration. Another common feature of the mutations in α-synuclein, Parkin, DJ-1, PINK1, and LRRK2 is the impairment in dopamine release and dopaminergic neurotransmission, which may be an early pathogenic precursor prior to death of dopaminergic neurons. Exposure to environmental and