Parkinson’s disease (PD) is the second most common neurodegenerative disease in the aging population, affecting about one million people in the United States and about ten million people worldwide1,2. PD is a progressive disease that primarily affects movement. Although PD itself is not fatal, complications from the disease are rated as the 14th cause of death in the United States2.
The cause of PD remains largely unknown but several factors are thought to play a role, including genetic mutations and environmental triggers (i.e. toxins, head injury, pesticide/herbicide exposure, occupation). Only about 10-15% of all PD cases are heritable forms of the disease with the remaining 85-90% classified as sporatic2, although it has recently been shown that genetic factors may still influence sporadic forms of the disease2,5. There are also notable histological changes in the brains of people with PD, including the presence of Lewy bodies that contain Alpha-synuclein, which cells cannot break down5.
PD is a chronic and progressive neurodegenerative disease that can manifest in both motor and non-motor symptoms that generally develop slowly over years. Most individuals with PD are diagnosed when they are 60 years or older, but early onset (diagnosis at 40 years or younger) affects about 2-10% of the one million people with PD in the United States1,2,3. There is even a rare form of PD called juvenile-onset Parkinson’s disease, which affects individuals prior to age 211.
PD is characterized by early and prominent cell death of the cells that produce dopamine in the substantia nigra1,3,4,5. Dopamine acts as a messenger between the substantia nigra and the corpus striatum. Dopaminergic communication between these two brain regions produces smooth and controlled motor movements1. As the level of dopamine decreases, communication between the substantia nigra and corpus striatum becomes ineffective and movement is impaired; the greater the loss of dopamine, the greater the level of impairment1,5. Unfortunately, by the time the first symptoms appear, individuals with PD will have lost 60-80% of the dopaminergic neurons in the substantia nigra1,3.
PD signs and symptoms vary from person to person and can include tremor, rigidity, bradykinesia (slowness of movement), stiffness, poor balance and coordination, speech and writing changes, as well as non-motor symptoms of anxiety, depression cognitive changes, hallucinations, delusions and dementia1,2,4,5. Although PD cannot be cured at this time, medications can markedly improve symptoms. More advanced cases of PD may require surgical interventions3,5.
PD is one of the most common neurodegenerative diseases in the aging population. Although it is known that that the lack of dopamine causes the symptoms and impairments in PD, many questions remain. For example, it is not known why the dopaminergic cells die1. Current treatment options also do not cure the disease5. Discovery and modification of the causes of the disease and the factors leading to disease progression will be the key in effective treatment for PD5. Bethyl manufactures many antibodies to proteins involved in PD that may aid in advancing breakthroughs and the development of effective treatments.
Below is the current listing of Bethyl antibodies involved in MAPK signaling pathway research: