I. the clinical features that distinguish PD

I.                  
Overview of
Parkinson’s disease

Parkinson’s disease is
a progressive condition involving dysfunction of dopamine-producing neurons in the
brain.  It considered the second most
common neurodegenerative disorder after Alzheimer’s disease. Importantly, the
clinical features that distinguish PD from other neurodegenerative diseases are
movement disorders, which associated with significant disability and
substantially decreased quality of life. Dopamine is a neurotransmitter that responsible
for body-coordinated movement, therefore the decreased levels of dopamine,
which characterized PDleads to difficulty with both voluntary and involuntary
movements.  It also involves nonmotor
symptoms such as depression, sleep disturbances, and orthostatic hypotension(Simuni & Sethi, 2008). The
pathologic hallmarks of the disease are degeneration of dopaminergic neurons in
the SNpc of the midbrain and the presence of Lewy bodies; cytoplasmic
aggregations of the protein ?-synuclein in brain neurons(Yamada et al., 2004). These features are associated with the
clinical signs of the disease (Nutt & Wooten, 2005).

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Interestingly, PDrepresented
0.3%of the general population worldwide, occurringin about 1% in individuals
aged 60 years or olderand increasing to about 4–5% of those aged 85years or
older(de Rijk et al., 2000; de Lau et al., 2004).

There is no known cause
for PD,although
a small percentage of patients may havea genetic form of the disorder.  Exposure tovarious toxins or pesticides may
be a secondaryetiology. The PD is likely a result ofmultiple factors, including
normal aging, geneticpredisposition, and environmental exposures.Interestingly, an age-related
decline of pigmented neurons inthe SNpchas beenobserved, with presence of Lewy
bodiesassociated with nigrostriatal dopamine depletion (Inzelberg et al., 2002; Chu & Kordower,
2007). Althoughmost patients with PD do nothave
a known family history of the disease, anincreasing number of genes or gene
loci havebeen associated with familial PD(Hague et al., 2005). Regarding to the environmental exposure, pesticides, herbicides
and other substances such as metals, solvents, paints, glues and living inrural
areas within industrialized countries significantly increased risk of
Parkinson’s(Priyadarshi et al., 2001; Inzelberg et al., 2002; Chade et al., 2006).Many researchers now believe that PD
results from a combination of genetic susceptibility and exposure to one or more
of environmental factors that trigger the disease. (Brown et al., 2006).

Additionally, lipophilic
drugs that deplete dopamine in the brain such as antipsychotics,
antidepressant, sedative, antiemetic and lithium drugs generally cause drug-induced
Parkinsonism (DIP),as DIP is condition that mimics PD. Characterized mainly by
rigidity and bradykinesia, it has less prominent tremor and gait instability. The
DIP is potentially reversible in addition; the severity and incidence of DIP
depend on the dosage and duration of exposure to such drug type.Therefore, the
best treatment of PID is removal of the provoking medication(Susatia & Fernandez, 2009).

On
the other hand, the pathological causemediating PDisloss of dopamine neurons in
the SN area of the brainstem that leads to depletion of dopamine in the corpus
striatum. Which are part of extrapyramidal motor system that control muscle
movement. The extrapyramidal motor system is a synchronization of pathways and
nerve tracts that connect the cerebral cortex, basal ganglia, thalamus,
cerebellum, reticular formation, and spinal neurons.  The corpus striatum consists of the caudate
nucleus and the lentiform nuclei that are made up of the putamen and the globus
pallidus. As dopamine neurons die, dopamine-relayedmessages cannot communicate
to other motor centers of thebrain, and patients develop motor symptoms.
Furthermore, other neurotransmitters in the basal ganglia such asacetylcholine,
histamine, glutamate, serotonin, dopamine,norepinephrine, epinephrine,
?-aminobutyric acid (GABA), enkephalins, substance P, and adenosinedecrease in
concentration as other brain regions degenerate. Interestingly, the decreases
in these neurotransmitters may explain some of the non motor symptoms of PD(Goetz, 2007; Truong et al., 2008; Lees et al., 2009).For example, loss of
dopamine and norepinephrineneurons in the limbic system is associated with
depressionand anxiety(Blonder & Slevin, 2011). Moreover, loss of
acetylcholine, dopamine, norepinephrine,and serotonin, in the SN, locus coeruleus,nucleus
raphe, and limbic system is associated with cognitiveimpairment(Blonder & Slevin, 2011).However,  the disease may begin in theautonomic system,
olfactory system, or vagus nerve in thelower brainstem and then spread to the
upper brainstem andcerebral hemisphere affecting dopamine pathways later inthe
course of disease progression(Lees et al.,
2009) . 

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