Parkinson’s disease is characterized by the neuronal accumulation of aggregated α-synuclein in the CNS and peripheral nervous system that results in a wide spectrum of worsening progressive motor and non-motor symptoms.
Mutations and changes in the levels of α-synuclein have been associated with multiple neurodegenerative illnesses, including Parkinson’s disease. The alpha-synuclein protein is a prominent component of Lewy bodies and Lewy neurites (abnormal protein clusters on the inside of neurons), the pathological hallmarks of several neurological disorders classified as synucleinopathies.
While diagnosis relies on motor symptoms classically associated with Parkinson’s disease, non-motor symptoms may present many years earlier.
Current treatments for Parkinson’s disease are symptomatic and only address a subset of symptoms such as motor impairment, dementia or psychosis. Symptomatic therapies do not target the underlying cause of the disease and lose effectiveness, often leading to debilitating side effects as the disease progresses. There are currently no treatments available that target the underlying cause of the disease and can slow or stop the progression.