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April 11-12, 2019 | Barcelona, Spain
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Neuroscience Congress 2019
Journal of Neurology and Neurorehabilitation Research | Volume 4
NEUROSCIENCE AND
NEUROLOGICAL DISORDERS
2
nd
International Conference on
PPARΒ/Δ ANTAGONISM RESCUES DOPAMINERGIC NEURONS IN AN IN VITRO
PARKINSON’S DISEASE MODEL
Andrea Antonosante
1
, Michele d’Angelo
1
, Elisabetta Benedetti
1
, Vanessa Castelli
1
, Cristiano Loredana
1
,
Mariano Catanesi
1
and
Cimini Annamaria
1,2,3
1
University of L’Aquila, Italy
2
Temple University, USA
3
Gran Sasso National Laboratory (LNGS), Italy
P
arkinson’s disease (PD) is one of the most common neurologic disorder. Motor dysfunctions are assigned
as primary symptoms of PD, being all related to events starting on one side of the body. Despite a relevant
number of studies, the mechanisms responsible for neurodegeneration in PD are still unknown, but oxidative
stress, excitotoxicity and neuroinflammation are believed to play key roles in neuronal death. The pathogenesis
of neurodegenerative diseases such as alzheimer’s disease (AD) and PD has also been described as reduced
neurotrophic support. There has been considerable interest in studying the involvement of neurotrophic fac-
tors, that are substances known to be crucial for the survival of specific neurochemical-phenotype classes of
neuron. We have previously reported that the peroxisomal proliferator activated receptor β/δ (PPARβ/δ) is in-
volved in the decrease of the TrkBFl in neurodegeneration. PPARs are a class of transcription factors involved in
the control of several pathways both in physiological and in pathological conditions including neurodegener-
ation. A detrimental role for PPARβ/δ has been proposed in AD, being closely related to the decrease of BDNF
andTrkBfl. On these bases, in the present work the signal transduction pathways activated in PDwere dissected
in two 6-OHDA in vitro models of PD (differentiated SH-SY5Y and LUHMES cells) treated with a PPARβ/δ specific
antagonist. The 6-OHDA treatments determined a significant increase of neuronal death, while the presence of
the antagonist rescued cell viability, thus indicating that blocking PPARβ/δ, neuronal survival pathways, such
as BDNF/TrkB, p-CREB, ERK5 were restored to control conditions.
J Neurol Neurorehabil Res 2019, Volume 4