作者: Maryam Moosavi , Rasoul Ghasemi , Asadollah Zarifkar , Karim Rastegar , Nader Maghsoudi
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摘要: BackgroundAlzheimer's disease (AD) is characterized by accumulation of intracellular neurofibrillary tangles (NTF) and senile plaques in the extracellular space and neuronal loss particularly in the hippocampus. Direct injection of preaggregated Aβ 25–35 or Aβ1–40/42 fragment are two nontransgenic in-vivo models frequently used to study the molecular, morphological and behavioral aspects of amyloid toxicity. Despite studies which have shown that intracerebral injection of Aβ 25–35 could induce molecular (like elevating caspase-3 activity, reactive gliosis and cell death) and behavioral changes, some authors reported that Aβ toxicity in vivo is not always reproducible, and some even believed that intracerebral injection of Aβ could not induce neurotoxic effects. This controversy often can be seen in rats and Aβ induction of AD in mice have less been questioned. For overwhelming this problem in rats …