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Parkinsons 2016
December 05-07, 2016
Volume 6 Issue 6(Suppl) J Alzheimers Dis Parkinsonism
ISSN: 2161-0460 JADP, an open access journal
conferenceseries .com
December 05-07, 2016 Phoenix, USA
2nd International Conference on
Parkinson’s Disease & Movement Disorders
J Alzheimers Dis Parkinsonism 2016, 6:6(Suppl)
Art is medicine: Combating Parkinson’s disease with creativity, positivity and movement
Saba M Shahid1,2
1Massasoit Community College, USA
2The American Parkinson’s Disease Association-Massachusetts Chapter, USA
People with Parkinson’s disease (PD) benefit from engaging in activities that promote creativity, relaxation and positivity. The
Art Cart’s Smile Trough Art Workshop is specifically designed to help those with PD explore their creativity by targeting
areas that are unique to this population. Our program includes modified equipment (easels, paint brushes, palates, etc.) which
has shown to meet the needs of PD participants more successfully than traditional art equipment. For the workshops we design
activities that will help this population combat the symptoms of PD such as tremors, rigidity of limbs, micrographia and loss
of fine motor control. While our paint dries, we encourage our participants to follow along and participate in exercises that
encourage strengthening of fine motor movement. After the culmination of each workshop, participants have the opportunity
to provide their feedback regarding the impact the art workshop had on them through a survey. As anticipated, those with
PD who participated in our Smile Through Art Workshop left with a heightened level of mood and an increased interest in
exploring their creativity. Thus far, 12 workshops have been programmed for the PD population in Massachusetts, targeting a
total of 26 participants. Nine (9) of the 12 workshops were offered through a continuous weekend program. Thus, it is believed
that engaging in art and promoting a healthy environment is beneficial and leaves those with PD and their caregivers with a
heightened quality of life.
Nilotinib effects in Parkinson’s disease and dementia with Lewy body
Charbel Moussa1, Fernando Pagan2, Michaeline Hebron1, Ellen H Valadez2, Yasar Tores-Yaghi2, Xu Huang1, Reversa R Mills2, Barbara M Wilmarth2,
Hellen Howard2 , Connell Dunn2, Alexis Carlson 2, Abigail Lawler 2, Sean L Rogers2, Ramsey (Drew) Falconer2, Jaeil Ahn1 and Zhaoxia Li1
1Georgetown University Medical Center, USA
2MedStar Georgetown Hospital, USA
C ancer and neurodegeneration include a group of diseases that are mechanistically distinct but may share common
therapeutic targets. Autophagy is a common quality control mechanism shared by mitotic and post-mitotic cells and
it can be exploited to accelerate clearance of unwanted oncogenes and reduce accumulation of toxic proteins in cancer and
neurodegeneration respectively. Tyrosine kinase inhibition is a therapeutically relevant strategy that can induce autophagy.
Our laboratory investigates TKIs that activate autophagy and are FDA-approved for cancer, thus significantly reducing research
and development efforts and cost by re-purposing. In neurodegeneration, the non- receptor tyrosine kinase ABL is activated.
Nilotinib and bosutinib are second generation BCR-ABL and SRC (short for Sacoma)-ABL inhibitors, respectively, that are
therapeutically used for individuals with leukemia. A fraction of nilotinib and bosutinib crosses the blood-brain barrier (BBB),
inhibits ABL and facilitates autophagic misfolded protein clearance, leading to neuroprotection and improved cognition and
motor behavior. Mice treated with a much lower dose of these drugs (< 25% of the typical leukemia dose) show significant
motor and cognitive improvement and degradation of misfolded proteins, leading to normal cell survival. We evaluated the
effects of low doses of Nilotinib, on safety and pharmacokinetics in Parkinson’s disease dementia or dementia with Lewy
body. Twelve subjects were randomized into 150 mg (N=5) or 300 mg (N=7) groups and received oral daily doses of nilotinib
for 24 weeks. The primary objectives were safety and tolerability; pharmacokinetics and target engagement were secondary,
while clinical outcomes were exploratory. This study shows that 150 mg and 300 mg daily doses of nilotinib are safe and well
tolerated in advanced Parkinson’s disease. Nilotinib is detected in the CSF and seems to engage the target via Abl inhibition.
Parkinson-related CSF biomarker, including homovanillic acid is significantly increased, DJ-1 is reduced and α-synuclein is
stable between baseline and 24-week nilotinib treatment. Exploratory cell death biomarkers including neuron specific enolase
and tau are also reduced. Motor and cognitive performance suggests stabilization of clinical outcomes. These data support the
potential of TKIs in the treatment of PD.