PARKINSON’S DISEASE: CIRCUIT-LEVEL PATHOPHYSIOLOGY AND CLINICAL MANIFESTATIONS
Authors
Alkov Ruslan Alimjonovich, Temirov Muhammad Alisher oʻgli, Boymurodova Oybarchin Saidmurod qizi ()Files
Abstract
Parkinson’s disease is a progressive neurodegenerative disorder characterized by core motor symptoms: bradykinesia, resting tremor, rigidity, and postural instability. The primary pathophysiological cause is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, depleting striatal dopamine and disrupting the balance between direct and indirect basal ganglia pathways. This leads to excessive output inhibition, abnormal beta-band synchronization, and suppressed thalamocortical drive. At the cellular level, the disease is marked by $\alpha$-synuclein accumulation (Lewy pathology), mitochondrial dysfunction, oxidative stress, and neuroinflammation. While dopamine replacement and deep brain stimulation targeting the subthalamic nucleus or globus pallidus effectively treat classic motor features, axial symptoms often persist due to non-dopaminergic neurodegeneration. Elucidating these circuit mechanisms remains vital for advancing disease-modifying therapies.
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