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Volume 8, Issue 6
J Neurol Neurosci
ISSN: 2171-6625 Neuro, an open access journal
Neuroscience 2017
October 16-17, 2017
OCTOBER 16-17, 2017 OSAKA, JAPAN
17
TH
Global Neuroscience Conference
Neurodegenerative diseases: A new view through iron homeostasis
Victor Manolov, Savina Hadjidekova, Julia Petrova, Vasil Vasilev, Maria Petrova, Yavor Jelev, Todor Kunchev, Petar Jeliazkov, Kamen Tzatchev and
Latchezar Traykov
Medical University in Sofia, Bulgaria
A
lzheimer’s Disease (AD), Parkinson’s Disease (PD) and Amyotrophic Lateral Sclerosis (ALS) are part of neurodegenerative
diseases. Their development is slow, progressive and most common is seen in elderly patients. Hepcidin leads to
iron deposition in neuronal structures as a result from oxidative stress. We tried to evaluate serum hepcidin levels in
neurodegenerative diseases and search for connection to disturbed iron homeostasis. 23 patients with AD, 17 cases with PD
and 13 with ALS were included, 24 males (45.3%). They were clinically and neurologically reviewed, EMG, IMT and ABI were
measured. They were evaluated for routine biochemical parameters and additional serum hepcidin were quantified. AAS,
nephelometric, ELISA and statistical methods were used during analyzes and obtained results interpretation. All results were
compared to age and gender matched healthy controls. We found statistically significant elevated serum hepcidin in patients
with neurodegenerative diseases (AD: 47.9±3.1 µg/L, PD: 49.8±5.1 µg/L, ALS: 53.8±4.9 µg/L) compared to healthy controls
(19.9±4.1 µg/L); P<0.001. Serum hepcidin correlates negatively to glutathione peroxidase and superoxide dismutase changes in
evaluated neurodegenerative diseases patients (0.9<r<0.7, P<0.05). Our findings support role of serum hepcidin quantification
as a marker for iron deposition in neurodegenerative diseases and might bring new view to early therapeutic implementation
in Alzheimer’s disease, Parkinson’s disease and amyotrophic lateralSclerosis.
victhedoc4@abv.bgJ Neurol Neurosci 2017, 8:6
DOI: 10.21767/2171-6625-C1-006