Therapeutic modification of alpha-synuclein

In a disease that ultimately involves much of the nervous system, small molecules that provide neuroprotection and neurorestoration to PD-affected brain areas represent the
most obvious therapeutic strategy. a-Syn is the major species composing Lewy bodies. The aberrant accumulation of a-syn likely plays a major role in the neurodegeneration
and progression of PD. From the standpoint that PD manifests as an a-synucleinopathy caused by an overabundance of the protein due to gene multiplication, associated
noncoding promoter variation that upregulates a-syn expression, or protein misfolding that results in enhanced fibrillization and decreased turnover spurred by any
number of factors, multiple levels of intervention in the disease
process may exist.