Final answer:
Parkinson's disease is characterized by the loss of dopaminergic neurons in the SNc, leading to dysarthria and other motor symptoms, and it involves cytoplasmic protein aggregates, mitochondrial dysfunction, oxidative stress, and glutamate excitotoxicity.
Step-by-step explanation:
Parkinson's Disease and Basal Ganglia Dysfunction
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNc), which project to the corpus striatum. This loss leads to a marked decrease in the neurotransmitter dopamine and results in movement disorders and cognitive changes. One of the symptoms that can arise due to dopaminergic depletion in the basal ganglia is a type of dysarthria, which is a motor speech disorder, often manifesting as slurred or slow speech. Treatments for PD typically aim to increase dopamine levels in the striatum to compensate for the loss of neurons, with L-DOPA being the most common medication, which serves as a precursor to dopamine. Unfortunately, there is a decreased responsiveness to this treatment over time.
The pathophysiology of PD includes the formation of cytoplasmic protein aggregates called Lewy bodies, predominantly composed of a-synuclein. Additionally, mitochondrial dysfunction, oxidative stress, and glutamate excitotoxicity have been implicated in the progression of PD. Symptoms such as bradykinesia, muscular rigidity, and tremors are tied to alterations in the basal ganglia circuitry due to dopaminergic denervation. Apart from motor symptoms, the disease also affects motivation and can lead to neuropsychiatric complications like depression and apathy.