Under many stress conditions, astrocytes often undergo drastic morphological changes. Hypertrophy of astrocytes is characterized by:
- Increased size of cell and soma
- Thicker processes
- Increased branching
For more information about astrocyte morphology, please see Astrocyte Morphology in Alzheimer’s Disease.
Hypertrophy of astrocytes due to brain ischemia. Astrocytes are shown in 3 regions, specifically in the contralateral hemisphere unaffected by the stroke, in the affected hemisphere but remote to the injury, and in the cortical infarct border zone. (A) Reactive astrogliosis is observed using GFAP immunostaining, with higher stain density and intensity closer to the injury. Scale bar = 20 μm. (B) 3D reconstruction of GFAP-labeled astrocytes imaged using confocal microscopy showing the increase in branching points, the thickening of the processes, and the increase in volume. Scale bar = 10 μm. Figures reproduced from Wagner et al. under the Creative Commons Attribution License.
References
Wagner et al., Acta Neurobiol. Exp., 73: 79–87, 2013; doi:10.55782/ane-2013-1923
Astrocytes are thought to play an important role in many neurogenerative diseases, such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Huntington’s disease, and Parkinson’s disease. Upon many stress conditions, astrocytes can undergo drastic morphological changes. Hypertrophy of astrocytes is generally characterized by an increase in the size of the cell and its soma, thicker processes, and increasing branching, as illustrated in the figure showing images of astrocytes as a function of distance to brain ischemia. In AD, hypotrophy of astrocytes has been observed in the early disease stages, prior to amyloid-β plaque accumulation, while hypertrophy of astrocytes has been observed after plaque accumulation.
To obtain a sensitive metric of the disease state, we have developed a fully-automated method for quantifying the astrocyte morphology in multiplex immunofluorescence (IF) images. In this presentation, we apply this method to study the disease progression in an APP/PS1 transgenic mouse model of AD.