Parkinson’s disease is a progressive neurological condition affecting movement, stemming from brain changes that lead to a range of symptoms. This article explores the biological differences between a healthy brain and one with Parkinson’s.
The Healthy Brain’s Motor Control System
The healthy brain controls smooth, coordinated movements through a network involving the basal ganglia. These deep brain structures process movement information and send refined instructions. The substantia nigra plays an important role in basal ganglia function.
The substantia nigra produces dopamine, a neurotransmitter that facilitates efficient communication between basal ganglia neurons. Dopamine is important for initiating and executing voluntary movements without stiffness. A balanced supply ensures movements are fluid, precise, and well-controlled, enabling activities like walking or writing.
Hallmarks of the Parkinson’s Brain
Parkinson’s disease involves structural and cellular brain changes. A primary characteristic is the degeneration and loss of dopamine-producing neurons within the substantia nigra. These cells progressively die, diminishing dopamine production.
Another feature is the presence of abnormal protein clumps called Lewy bodies. These deposits are composed of misfolded alpha-synuclein protein, accumulating inside brain cells. Found in various brain regions, Lewy bodies are notable in the substantia nigra, where they are thought to interfere with normal brain function. Their exact role in disease progression is still under investigation.
Neurotransmitter Imbalances in Parkinson’s
Structural damage in Parkinson’s brains leads to reduced dopamine levels. As substantia nigra neurons degenerate, the brain’s ability to synthesize and release dopamine is compromised. This deficiency disrupts basal ganglia communication, impacting movement regulation.
Other neurotransmitter systems can also be affected. Parkinson’s patients often lose nerve endings producing norepinephrine, a neurotransmitter for automatic bodily functions like pulse and blood pressure. This reduction may contribute to non-motor symptoms like fatigue and blood pressure changes. While dopamine is the primary focus due to its link to motor control, other neurotransmitters’ involvement highlights the disease’s widespread impact on brain chemistry.
Translating Brain Changes to Symptoms
Anatomical and neurochemical changes in the Parkinson’s brain lead to observable symptoms. Progressive loss of dopamine-producing neurons in the substantia nigra and resulting dopamine deficiency cause characteristic motor symptoms. These include resting tremor (involuntary shaking of a limb at rest). Slowness of movement (bradykinesia) makes initiating and executing movements difficult, such as taking the first step or buttoning a shirt.
Muscle rigidity (stiffness) is another common motor symptom arising from disrupted motor control pathways. As the disease progresses, postural instability develops, causing balance problems and increased fall risk. Beyond motor symptoms, broader brain involvement, including Lewy bodies and other neurotransmitter imbalances, contributes to non-motor symptoms. These include sleep disturbances, cognitive changes, loss of smell, depression, and constipation, reflecting the disease’s widespread impact on brain functions.