Fariha Jamal is an Assistant Professor, Department of Neurology, Baylor College of Medicine and an Assistant Clinical Director at the Parkinson’s Disease Research Education and Clinical Center, Michael E. DeBakey VA Medical Center in Houston, Texas. Correspondence: Fariha Jamal (fariha.zaheer@bcm.edu)
Author Disclosures The author reports no actual or potential conflicts of interest with regard to this article.
Disclaimer The opinions expressed herein are those of the author and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.
Background: Parkinson disease (PD) is a progressive neurodegenerative disorder. Pathologic diagnosis of PD relies on loss of dopamine neurons in the substantia nigra and accumulation of the abnormal protein α -synuclein in the form of Lewy bodies and Lewy neurites. Alteration in aggregation properties of this protein is believed to play a central role in the pathogenesis of PD.
Observations: Huge interest has developed in antibody-based therapies for PD. Several studies have tested immunotherapies in PD animal models with the aim of targeting α -synuclein. Immunotherapies can be instituted in 2 ways: active immunization in which the immune system is stimulated to produce antibodies against α -synuclein or passive immunization in which antibodies against α -synuclein are directly administered.
Conclusions: Immunotherapy against α -synuclein has provided a new therapeutic avenue in neuroprotection. Results from the first human clinical trial are promising, but despite these results, more work is needed to clarify the role of α -synuclein in the pathogenesis of PD in humans.
Parkinson disease (PD) is a progressive neurodegenerative disorder, characterized by diverse clinical symptoms. PD can present with rest tremor, bradykinesia, rigidity, falls, postural instability, and multiple nonmotor symptoms.Marras and colleagues estimated in a comprehensive meta-analysis that there were 680,000 individuals with PD in the US in 2010; this number is expected to double by 2030 based on the US Census Bureau population projections.1 An estimated 110,000 veterans may be affected by PD; hence, understanding of PD pathology, clinical progression, and effective treatment strategies is of paramount importance to the Veterans Health Administration (VHA).2
The exact pathogenesis underlying clinical features is still being studied. Pathologic diagnosis of PD relies on loss of dopamine neurons in the substantia nigra and accumulation of the abnormal protein, α-synuclein, in the form of Lewy bodies and Lewy neurites. Lewy bodies and neurites accumulate predominantly in the substantia nigra in addition to other brain stem nuclei and cerebral cortex. Lewy bodies are intraneuronal inclusions with a hyaline core and a pale peripheral halo. Central core stains positive for α-synuclein.3,4 Lewy neurites are widespread and are believed to play a larger role in the pathogenesis of PD compared with those of Lewy bodies.5
