AI Article Synopsis

  • Recent research highlights the role of glial cells, particularly astrocytes, in the progression of neurodegenerative diseases like Alzheimer's, moving beyond the traditional focus solely on neurons.
  • Reactive astrogliosis describes the changes that astrocytes undergo in response to tissue damage, which can result in disease-specific astrocyte phenotypes.
  • The study of neurotoxic astrocytes in a triple transgenic mouse model of Alzheimer’s disease reveals that their altered functions may lead to harmful outcomes for neurons and could be linked to stress responses and metabolic changes in the brain's environment.

Article Abstract

Neurodegenerative diseases such as Alzheimer's disease have been classically studied from a purely neuronocentric point of view. More recent evidences support the notion that other cell populations are involved in disease progression. In this sense, the possible pathogenic role of glial cells like astrocytes is increasingly being recognized. Once faced with tissue damage signals and other stimuli present in disease environments, astrocytes suffer many morphological and functional changes, a process referred as reactive astrogliosis. Studies from murine models and humans suggest that these complex and heterogeneous responses could manifest as disease-specific astrocyte phenotypes. Clear understanding of disease-associated astrocytes is a necessary step to fully disclose neurodegenerative processes, aiding in the design of new therapeutic and diagnostic strategies. In this work, we present the transcriptomics characterization of neurotoxic astrocytic cultures isolated from adult symptomatic animals of the triple transgenic mouse model of Alzheimer's disease (3xTg-AD). According to the observed profile, 3xTg-AD neurotoxic astrocytes show various reactivity features including alteration of the extracellular matrix and release of pro-inflammatory and proliferative factors that could result in harmful effects to neurons. Moreover, these alterations could be a consequence of stress responses at the endoplasmic reticulum and mitochondria as well as of concomitant metabolic adaptations. Present results support the hypothesis that adaptive changes of astrocytic function induced by a stressed microenvironment could later promote harmful astrocyte phenotypes and further accelerate or induce neurodegenerative processes.

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http://dx.doi.org/10.1007/s12031-023-02105-2DOI Listing

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