IMR Press / FBL / Volume 7 / Issue 1 / DOI: 10.2741/tabira

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Significance of intracellular Aβ42 accumulation in Alzheimer's disease

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1 National Institute for Longevity Sciences, Obu, Aichi 474-8522
2 Laboratory for Alzheimer Disease, Riken Brain Science Institute, Wako, Saitama 351-0198
3 Department of Neuropsychiatry, Okayama University Medical School, Okayama 700- 8558, Japan
Academic Editor:Mark M. Smith
Front. Biosci. (Landmark Ed) 2002, 7(1), 44–49;
Published: 1 April 2002
(This article belongs to the Special Issue Alzheimers disease)

Aβ plays a pivotal role in the pathogenesis of Alzheimer's disease (AD), but it is still obscure how it causes AD. We have established transgenic mice carrying wild-type or familial Alzheimer's disease (FAD) mutant-type presenilin 1 (PS1). In these mice, the number of cortical and hippocampal neurons decreased along with age in mutant mice. In addition, the old mutant mice showed a significant increase of dark neurons by silver staining and the number of neurons with intracellular Aβ42 by immunohistochemistry. Our extended study also showed a significant increase of intracellular Aβ42-positive neurons in isolated cases of AD as well as in PS1 mutant FAD cases. These neurons frequently showed apoptotic staining. However, coincidence of apoptotic markers and intraneuronal neurofibrillary tangles (NFT) was insignificant. Notably intraneuronal Aβ42-labeling was frequently seen in a case of AD showing cotton-wool type senile plaques with a few NFT positive neurons and dystrophic neurites. These results indicate that intraneuronal deposition of Aβ42 is important in the pathogenesis of AD.

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