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uhe purpose of the study was to evaluate the effects of conventional and sustained
delivery of levodopa (L-dopa) alone or in combination with acetylcholine in SH-SY5Y
neuroblastoma cells. uhe loss of dopaminergic neurons resulting in an imbalance
between dopamine and acetylcholine is a hallmark feature of Parkinson disease. L-
dopa has been shown to potentiate D2 receptor-mediated effects and inhibits
acetylcholine release in Parkinson disease. According to the literature, conventionally
administered L-dopa is short-lived and oxidized to metabolites which are neurotoxic
and lead to a further decline in dopaminergic neurons. In addition, most in vitro
studies do not taken into account that acetylcholine is elevated in vivo. SH-SY5Y cells
were conventionally administered or in a sustained manner L-dopa, acetylcholine, or
a combination of acetycholine and L-dopa for periods of 24, 48 and 72 hours, and
evaluated for cell proliferation, cell viability, cellular damage, nitric oxide production,
cellular glutathione levels, and hydrogen peroxide production. Overall, sustained
delivery of L-dopa alone or in combination with acetylcholine showed decreases in
cell number which were 50% less than those seen by conventional administration of
the compounds within the first 48 hours of culture. However, regardless of
administration of L-dopa alone or in combination with acetylcholine there were
increases in cellular levels of MDA, nitric oxide, and hydrogen peroxide. Interestingly,
the increases seen in the sustained delivery of L-dopa were less than those seen with
conventional administration. In addition, the increased levels of the aforementioned
parameters were delayed by 24 hours compared with conventional administration of
these compounds. Appearances of the culture media following sustained delivery
show increased in oxidized L-dopa. It is more than likely that the decreases in cell
number and increased levels of nitric oxide, hydrogen peroxide, and MDA are a direct
result of the oxidized metabolites of L-dopa.

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uhe aim of this study is to analyze executive function and motor symptoms in
patients with idiopathic Parkinson's disease (PD). uhe sample consisted of 44 subjects
with PD between the ages of 45 to 75, who were examined consecutively. uhe
subjects were divided into two groups according to the duration of the disease. uhe
control group was composed of spouses, family and accompanying members.
Patients included were submitted to motor dysfunction evaluation using the UPDRS.
uhe executive functions modalities analyzed included: operational memory, inhibitory
control, planning, cognitive flexibility and inductive reasoning. Significant differences
between the experimental and control groups were found in all the executive
domains studied. Evidence of tremor, rigidity and bradykinesia correlation with
executive dysfunction were not observed. Patients with PD, even in the initial phase
of the disease, presented executive dysfunction. uhe cardinal motor signs of the
disease were not correlated with the cognitive dysfunction found%V
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Oxidative stress plays a central role in neuronal injury and cell death in acute and
chronic pathological conditions. uhe cellular responses to oxidative stress embrace
changes in mitochondria and other organelles, notably endoplasmic reticulum, and
can lead to a number of cell death paradigms, which cover a spectrum from
apoptosis to necrosis and include autophagy. In Alzheimer's disease, and other
pathologies including Parkinson's disease, protein aggregation provides further
cellular stresses that can initiate or feed into the pathways to cell death engendered
by oxidative stress. Specific attention is paid here to mitochondrial dysfunction and
programmed cell death, and the diverse modes of cell death mediated by
mitochondria under oxidative stress. Novel insights into cellular responses to
neuronal oxidative stress from a range of different stressors can be gained by
detailed transcriptomics analyses. Such studies at the cellular level provide the key
for understanding the molecular and cellular pathways whereby neurons respond to
oxidative stress and undergo injury and death. uhese considerations underpin the
development of detailed knowledge in more complex integrated systems, up to the
intact human bearing the neuropathology, facilitating therapeutic advances.
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uhe role of the AuP-gated receptor, P2X(7), has been evaluated in the unilateral 6-
OHDA rat model of Parkinson's disease using the P2X(7) competitive antagonist A-
438079. Nigral P2X(7) immunoreactivity was mainly located in microglia but also in
astroglia. A-438079 partially but significantly prevented the 6-OHDA-induced
depletion of striatal DA stores. However, this was not associated with a reduction of
DA cell loss. Blockade of P2X(7) receptors may represent a novel protective strategy
for striatal DA terminals in Parkinson's disease and warrants further future
investigationV

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Dopaminergic (DA) agonist-induced yawning in rats seems to be mediated by DA D3
receptors, and low doses of several DA agonists decrease locomotor activity, an
effect attributed to presynaptic D2 receptors. Effects of several DA agonists on
yawning and locomotor activity were examined in rats and mice. Yawning was
reliably produced in rats, and by the cholinergic agonist, physostigmine, in both the
species. However, DA agonists were ineffective in producing yawning in Swiss-
Webster or DA D2R and DA D3R knockout or wild-type mice. uhe drugs significantly
decreased locomotor activity in rats at one or two low doses, with activity returning
to control levels at higher doses. In mice, the drugs decreased locomotion across a
1000-10 000-fold range of doses, with activity at control levels (U-91356A) or above
control levels [(+/-)-7-hydroxy-2-dipropylaminotetralin HBr, quinpirole] at the highest
doses. Low doses of agonists decreased locomotion in all mice except the DA D2R
knockout mice, but were not antagonized by DA D2R or D3R antagonists (L-741 626,
BP 897, or PG01037). Yawning does not provide a selective in-vivo indicator of DA
D3R agonist activity in mice. Decreases in mouse locomotor activity by the DA
agonists seem to be mediated by D2 DA receptors.

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ŒŒŒŒŒŒŒŒŒŒŒ ŒŒŒŒŒŒŒŒŒŒŒŒŒŒŒ ŒŒŒŒŒŒŒă茌  ŒŒŒŒŒŒŒ
ŒŒŒŒŒŒŒŒŒŒŒŒ ŒŒ  
 

ŒŒŒŒŒŒŒŒŒŒ Œè Œ Œ ŒŒŒŒŒŒŒŒŒŒŒŒŒŒŒŒŒ ŒŒŒŒŒŒŒŒă ŒŒ ŒŒ
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