Previous Page  19 / 21 Next Page
Information
Show Menu
Previous Page 19 / 21 Next Page
Page Background

Page 78

conferenceseries

.com

Volume 8

Journal of Alzheimers Disease & Parkinsonism

ISSN: 2161-0460

Dementia 2018

October 29-31, 2018

October 29-31, 2018 | Valencia, Spain

12

th

International Conference on

Alzheimer’s Disease & Dementia

Intranasal insulin attenuate signs of Alzheimer’s disease following chronic hypoxia

Simin Mahakizadeh

Tehran University of Medical Sciences, Iran

A

lzheimer’s disease (AD) is a metabolic neurodegenerative disease featured by cerebrovascular dysfunction in addition to

cognitive decline. Amyloid β (Aβ) plaques followed by up-regulation of amyloid precursor protein (APP) and seladin-1

down-regulation, as well as insulin signaling impairment are associated with this disease. This study was designed to evaluate

the effect of insulin on Alzheimer’s signs induced by chronic hypoxia. 24 male rats were randomly divided into four groups:

control (C), sham (Sh), hypoxia (H), hypoxia + insulin (HI) and were exposed to hypoxic chamber (8% O2, 92% N2) for 30

days (four hours/day) in H and HI groups. Pro-inflammatory cytokines and insulin receptor substrate (IRS-1) in sera were

measured on day 30 after hypoxia period. Intranasal insulin administration was used as a neuroprotective and antidiabetic

drug. Spatial learning and memory were analyzed using the Morris water maze task. Amyloid precursor protein gene (APP)

and seladin-1 gene expression were studied in the hippocampus by real time-PCR. TNF-α, IL-1β and IRS-1 had significant

magnification in H group compared with C and Sh groups (p<0.05). Insulin improved Alzheimer’s signs such as seladin-1

fallen, APP risen gene expression and memory impairment. In conclusion, we indicate that chronic hypoxia mediates AD

pathogenesis and using insulin hormone as a neuroprotective and antidiabetic drug could be beneficial in neurodegenerative

damage induced by hypoxia.

Si.mahakizadeh@gmail.com

J Alzheimers Dis Parkinsonism 2018, Volume 8

DOI: 10.4172/2161-0460-C7-055