The clinical features historically associated with PD are the triad of motor symptoms, namely, tremor, rigidity, and bradykinesia, with postural instability often appearing as the disease progresses. As our understanding of the pathogenesis of PD increases and more is learned about new therapeutic targets, the potential for the development of disease-modifying therapies is promising. Yet, further investigation on novel therapies to reduce the rate of neurodegeneration or even to replenish the loss of dopaminergic cells remains in the research setting, with some in the early stages of clinical trials. However, as dopamine is not the only neurotransmitter involved in PD, many other drugs are also being used to target specific symptoms, such as depression or dementia. Treatment predominantly focuses on symptomatic relief with drugs aiming to either restore the level of dopamine in the striatum or to act on striatal post-synaptic dopamine receptors. Clinical criteria, however, can only lead to a diagnosis of probable PD, while a definitive diagnosis requires histopathological assessment, with the identification of α-synuclein-containing Lewy bodies (LBs) or Lewy neurites. Currently, diagnosis is based on clinical symptoms with the criteria for a diagnosis requiring the presence of two of the following clinical features: resting tremor, bradykinesia, rigidity and/or postural instability. Such a widespread pathology makes PD a very heterogeneous disorder, and a reliable diagnostic test is not yet available. ![]() PD is pathologically characterized by the loss of nigrostriatal dopaminergic innervation, although neurodegeneration is not limited to only the nigral dopaminergic neurons but also involves cells located in other regions of the neural network. With an aging population, both the prevalence and incidence of PD are expected to increase by more than 30% by 2030 ( 4), which will result in both direct and indirect costs on both society and the economy as a whole. ![]() PD is the second most common neurodegenerative disease after Alzheimer’s disease (AD) ( 1), with a prevalence of approximately 0.5–1% among those 65–69 years of age, rising to 1–3% among persons 80 years of age and older ( 2, 3). It was first described by James Parkinson in 1817 and further characterized by Jean-Martin Charcot, and our knowledge of PD is continuing to expand. Parkinson’s disease (PD) is a complex progressive neurodegenerative disease characterized by tremor, rigidity, and bradykinesia, with postural instability appearing in some patients as the disease progresses. Several processes have been implicated in PD, including mitochondrial dysfunction, defective protein clearance mechanisms, and neuroinflammation, but the way in which these factors interact remains incompletely understood. The movement disorder arises due to the loss of dopaminergic neurons of the substantia nigra pars compacta, with the pathological hallmark being intracellular aggregates of α-synuclein, in the form of Lewy bodies and Lewy neurites. Environmental influences such as smoking, caffeine consumption, and pesticide exposure have been postulated to alter the risk of PD development, although the role of these remains unclear. The cause of PD is not known, but a number of genetic risk factors have now been characterized, as well as several genes which cause rare familial forms of PD. While a number of non-motor manifestations arise, the typical clinical features involve a movement disorder consisting of bradykinesia, resting tremor, and rigidity, with postural instability occurring at a later stage. Parkinson’s disease (PD) is a common neurodegenerative disorder.
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