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Neuro Congress 2019 Journal of Brain and Neurology | Volume 3
Page 15
June 19-20, 2019 | Dublin, Ireland
OF EXCELLENCE
IN INTERNATIONAL
MEETINGS
YEARS
NEUROLOGY AND BRAIN DISORDERS
3rd International Conference on
ALTERED HEME IRON HOMEOSTASIS IN
ALZHEIMER’S DISEASE
Mitochondrial dysfunction and bioenergetic deficits have been identi-
fied as early and potentially causative events in Alzheimer’s disease
(AD) pathogenesis. Importantly, heme is a key factor in mitochondrial func-
tion and bioenergetics. Heme is a central metabolic and signaling mole-
cule regulating diverse molecular and cellular processes relating to oxygen
utilization and metabolism. Heme serves as a prosthetic group in proteins
and enzymes involved in oxygen transport, utilization and storage such as
globin’s and cytochromes. Multiple subunits in mitochondrial respiration or
oxidative phosphorylation (OXPHOS) complexes II-IV contain heme. Further,
heme acts as a signaling molecule to coordinate the expression of genes en-
coding globins and cytochromes as well as the translocation and assembly
of these protein/enzyme complexes. Heme binds to and directly regulates
the activities of many proteins controlling processes ranging from tyrosine
kinase signaling to microRNA processing. Thus, researchers assessed the im-
portance of altered heme metabolism in AD pathogenesis. To investigate the
role of altered hememetabolism in AD, they identified heme-related proteins
whose expression is altered in AD patients andmouse models exhibiting am-
yloid pathology. They detected the levels of proteins involved in heme syn-
thesis, uptake degradation and function during neuronal differentiation and
characterized the effects of Aβ. They found that the expression levels of the
rate-limiting heme synthetic enzyme ALAS1 and heme degradation enzyme
HO-2 are selectively decreased in AD patients andmice. Aβ selectively reduc-
es the levels of HO-2 and heme degradation, which are elevated to support
neuronal functions in fully differentiated neuronal cells. Our data show that
lowered heme metabolism, particularly the decreased levels of heme degra-
dation and HO-2 are likely a very early event in AD pathogenesis.
Li Zhang, J Brain Neurol 2019, Volume 3
Li Zhang completed her PhD at UCLA and Post-
doctoral studies at the MIT Department of Biolo-
gy. She is the Cecil H and Ida Green Distinguished
Chair in Systems Biology Science at the Universi-
ty of Texas at Dallas. Her laboratory has studied
heme signaling and function for 20+ years and
published many original research articles and a
book entitled “HEME BIOLOGY: THE SECRET LIFE
OF HEME IN REGULATING DIVERSE BIOLOGICAL
PROCESSES” on this subject. Her laboratory has
also helped unravel the functions of molecular
chaperones, oxygen signaling and the actions
of neurotoxicants. Her research interest is to elu-
cidate the molecular events underlying altered
heme iron homeostasis in AD pathogenesis and
lung tumorigenesis.
Li Zhang
University of Texas at Dallas, USA
BIOGRAPHY
Keynote Forum | Day 1