Brain iron overload has been implicated in the pathology of Parkinson disease; this aspect of the disease is recapitulated in Drosophila models of the disease. Using several different fly models of Parkinson disease, the efficacy of different iron-chelating therapeutics has been assessed and a downstream gene linking iron toxicity to mitochondrial dysfunction has been identified.
[updated Aug. 2018 by FlyBase; FBrf0222196]
Parkinson disease (PD) is a neurodegenerative disease usually typified by slow onset in mid to late adulthood; there are also early-onset and juvenile forms of the disease. Symptoms worsen over time and include resting tremor, muscular rigidity, bradykinesia [abnormal slowness of movement], and postural instability [impaired balance and coordination]; additional symptoms may include postural abnormalities, dysautonomia [symptoms caused by malfunction of the autonomic nervous system], dystonic cramps, and dementia. Parkinson disease is the second-most common neurodegenerative disease (after Alzheimer disease), affecting approximately 1% of the population over 50 (Polymeropoulos et al., 1996, pubmed:8895469). [from MIM:168600; 2013.07.23]
Parkinson disease is described as early-onset disease if signs and symptoms begin before age 50. Early-onset cases that begin before age 20 may be referred to as juvenile-onset disease. [from Genetics Home Reference, GHR_condition:parkinson-disease, 2015.02.13]
Iron overload has been implicated in the pathology and pathogenesis of Parkinson's disease (PD). The substantia nigra, where the selective loss of dopaminergic neurons occurs, is the primary region in the brain known to deposit iron (Wang et al., 2016; pubmed:27827408).
