Paper Information

Title: 

FIBRILLAR BETA-AMYLOID (AΒ) (1-42) ELEVATES EXTRACELLULAR AΒ IN CULTURED HIPPOCAMPAL NEURONS OF ADULT RATS

Type: POSTER
Author(s): RASTGAR K.,MAJD SH.,ZARIFKAR A.A.,TAKHSHID M.A.
 
 
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: Alzheimer's disease (AD) is a chronic disorder with progressive neurodegeneration associated with aging and is characterized by fibrillar beta-amyloid (Aβ) deposits in the brain. Although, the increased production of Aβ seems to play a noticeable role in AD pathogenesis and its progression, all the mechanisms which are involved in this extracellular Aβ elevation are not known completely.
Methods: We used adult neuronal culture as an in vitro model which is favorable for adult neurodegenerative diseases studies. We introduced a toxic concentration for fibrillar Aβ1-42 in adult neurons which was much lower from the toxic concentration in embryonic neurons. We determined the effect of fibrillar Aβ1-42, as the most toxic part of amyloid plaques, in extracellular Aβ1-40, as the main part of Aβ plaques. We treated the neurons with fibrillar Aβ1-42 in nontoxic concentrations of 2×10-6μM, 2×10-5μM and 2×10-4μM and measured extracellular Aβ1-40. Results: Our findings show that even very low levels of fibrillar Aβ1-42 can contribute to subsequent extracellular Aβ elevation in a dose dependent manner. Conclusion: These results suggest that even low levels of fibrillar Aβ may have deleterious actions if it remains in extracellular space for a period of time.

 
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