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conferenceseries.com
October 26-27, 2016 Chicago, USA
Annual Congress on
Rare Diseases & Orphan Drugs
Volume 7, Issue 5 (Suppl) J Genet Syndr Gene Ther
ISSN: 2157-7412 JGSGT, an open access journal Rare Diseases 2016
October 26-27, 2016
Failures in brain energy metabolism unveil therapeutic targets for Huntington’s disease
Maite A Castro
Universidad Austral de Chile, Chile
The brain makes up 2% of a person's weight. Despite this, even at rest, the brain consumes 25% of the body's energy. Most of
the energy consumed in the brain is attributable to restoration of the membrane gradient following neuronal depolarization.
Neurotransmitter recycling, intracellular signaling and dendritic and axonal transport also require energy. Even though neurons are
responsible for massive energy consumption, the brain is made up of many cells, including neurons, glial and ependymal cells. Every
brain cell has a specific function and thus every brain cell has different metabolic needs. Many of these specific functions are concerned
with maintenance of neuronal transmission. Astrocytes play a central role in supporting neurons metabolically by producing lactate,
through glycolysis and activation of glycogen catabolism. There have been several reports of metabolic impairment in a variety of
neurodegenerative disorders such as Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis and Parkinson's disease,
among others. Moreover, deregulation of energy metabolism could be implicated in an increased production of oxidative species.
During the last 10 years we have been making steady progress in the mechanisms of communication between neurons and glial cells,
the way they regulate their metabolism and the use of ascorbic acid as inter cellular messenger. Here, we will describe the regulation of
neuronal glucose, lactate and ascorbic acid transporters under synaptic activity in mice models of Huntington's disease. Experiments
demonstrating a failure in astrocytic ascorbic acid recycling and ascorbic acid-dependent modulation on neuronal metabolism in
Huntington's disease will be discuss. Brain is an expensive organ in energetic terms so disruptions in energy production may affect
neuronal transmission and thus, neuronal survival.
Biography
Maite A Castro is a Professor in the Department of Biochemistry at the Universidad Austral de Chile since 2005. She has obtained her PhD in Biological Sciences at
Universidad Austral de Chile in 2005. In 2009, she did a Postdoctoral training in Dr. Michael Levine’s Laboratory at the University of California, Los Angeles, USA.
During the last 15 years she has been making steady progress in the mechanisms of communication between neurons and glial cells and the way they regulate
their metabolism. Presently, her interest is to study the correlation between failures in brain energy metabolism and the progression of Huntington disease.
Maite A Castro, J Genet Syndr Gene Ther 2016, 7:5 (Suppl)