Vol. 122, No. 1 (Supplement) 2017
Supplement abstract

Astrocyte clasmatodendrosis in a transgenic mouse model of Alzheimer’s Disease

Published 2017-10-06


  • Clasmatodendosis,
  • Alzheimer's Disease,
  • Aß-fibril,
  • Astrocytes

How to Cite

Nosi, D., Lana, D., Giovannini, M., Casamenti, F., & Zecchi Orlandini, S. (2017). Astrocyte clasmatodendrosis in a transgenic mouse model of Alzheimer’s Disease. Italian Journal of Anatomy and Embryology, 122(1), 157. Retrieved from https://oajournals.fupress.net/index.php/ijae/article/view/2005


Aging is frequently accompanied by a low-grade inflammation (inflammaging); on the other hand, inflammation is considered a prodrome of Alzheimer Disease (AD). Indeed, a distinctive event of both aging and AD is the deposition of beta amyloid (Aß) fibrils within the central nervous system, a condition that has been associated to cognitive decline. In a previous research we demonstrated that, in the hippocampus of aged rats, the fragmentation of astrocyte processes (clasmatodendrosis) is associated with a decrease of their activity in terms of Aß-fibril clearance, thus promoting neuron to neuron propagation of Aß-fibrils and therefore their prion like spread [1]. In this study we show preliminary data on the role of clasmatodendrosis in a double transgenic TgCRND8 mouse model, which overexpresses both Swedish and Indiana mutations in the human amyloid precursor protein, and displays early cognitive decline also in young animals [2]. We performed a 3D confocal analysis on optical volumes acquired in the CA1 hippocampal region of young (3m.)- and middle aged (7m)- TgCRND8 mice. We found that young TgCRND8 mice show Aß-amyloid deposition, astrocyte clasmatodendrosis and a decrease of the astrocyte cytoskeletal marker GFAP. In middle aged animals significantly higher levels of GFAP expression, indicating astrogliosis, were in concomitance with both Aß-amyloid deposition. These data appear to link the onset of early cognitive decline in TgCRND8 mice with astrocyte clasmatodendrosis and provide new perspectives on the role of astrocytes in Aß-amyloid deposition and spreading.