Luteinizing Hormone, a Reproductive Regulator That Modulates the Processing of Amyloid- Precursor Protein and Amyloid- Deposition*

نویسندگان

  • Richard L. Bowen
  • Giuseppe Verdile
  • Tianbing Liu
  • Albert F. Parlow
  • George Perry
  • Mark A. Smith
  • Ralph N. Martins
  • Craig S. Atwood
چکیده

From Voyager Pharmaceutical Corporation, Raleigh, North Carolina 27615, the Centre for Aging and Alzheimer’s Disease, School of Biomedical and Sports Science, Edith Cowan University, Joondalup, Western Australia 6027, Australia, the Department of Psychiatry and Clinical Neurosciences, The University of Western Australia and The Sir James McCusker Alzheimer’s Disease Research Unit, Hollywood Private Hospital, Perth, Western Australia 6009, Australia, the Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison, Wisconsin 53705, the National Hormone and Peptide Program, Harbor-UCLA Medical Center, Torrance, California 90509, the Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, and the Department of Medicine, University of Wisconsin, Madison, Wisconsin 53705

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Luteinizing hormone modulates cognition and amyloid-beta deposition in Alzheimer APP transgenic mice.

Until recently, the study of hormonal influences in Alzheimer disease was limited to the role of sex steroids. Despite numerous epidemiological studies supporting a protective role for estrogen in Alzheimer disease, recent studies show that estrogen administration in elderly women increases the risk of disease. Reconciling these contradictory reports, we previously hypothesized that other hormo...

متن کامل

The contribution of luteinizing hormone to Alzheimer disease pathogenesis.

Several hypotheses have been proposed that attempt to explain the pathogenesis of Alzheimer Disease (AD) including theories involving senile plaque and neurofibrillary tangle formation, increased oxidative stress, and cell cycle abnormalities, since evidence for each of these pathological phenomena have been well documented in AD. Recent epidemiological and experimental data also support a role...

متن کامل

Effect of Long-term Exposure to Extremely Low-frequency Electromagnetic Fields on β-amyloid Deposition and Microglia Cells in an Alzheimer Model in Rats

Background: Recently, researchers have considered extremely low-frequency electromagnetic fields (ELF-EMFs), as one of the non-invasive therapies, in the treatment of many severe neurological disorders, including Alzheimer Disease (AD). AD is a progressive neurodegenerative disease characterized by the deposition of amyloid plaques in the brain. However, the increase in microglial cells increas...

متن کامل

Cholinergic neuropathology in a mouse model of Alzheimer's disease

Transgenic mice over-expressing mutant human amyloid precursor protein (PDAPP mouse) develop several Alzheimer’s disease (AD)-like lesions including an age-related accumulation of amyloid-?-containing neuritic plaques. Although aged, heterozygous PDAPP mice also exhibit synaptic and glial cell changes, that is characteristic of AD pathology, no evidence of neurodegeneration has been observed. T...

متن کامل

Investigation of the Iron Oxide Nanoparticle Effects on Amyloid Precursor Protein Processing in Hippocampal Cells

Introduction: Iron oxide nanoparticles (Fe2O3-NPs) are small magnetic particles that widely used in different aspects of biology and medicine in modern life. Fe2O3-NP accumulated in the living cells due to absence of active system to excrete the iron ions so damages cellular organelles by highly reactivity. Method: Herein cytotoxic effects of Fe2O3-NP with 50 nm size were investigated on prima...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2004