About this Research Topic
The involvement of glial cells in Alzheimer's disease (AD) has been mostly viewed as a secondary adaptive response to neuronal pathology. However, it emerges that dysfunctional glial cells can initiate and worsen neuronal dysfunction. This leads to increased inflammation, deficient neuroprotection, reduced clearance of protein aggregates, and impaired synaptic function. These features, in turn, collectively contribute to the development and progression of AD pathology by mechanisms including:
1. Inflammation: In response to the buildup of protein aggregates such as amyloid-β plaques, glial cells become activated, release inflammatory cytokines, and send and receive complement-related signals, which together may exacerbate the damage caused by the plaques.
2. Neuroprotection: Glial cells, in particular astrocytes, provide neuroprotection by releasing metabolites, growth factors, and antioxidants, which help reduce oxidative stress and protect neurons in physiological conditions. In AD, these neuroprotective mechanisms are compromised, leading to excessive damage to neurons.
3. Clearance of protein aggregates: Glial cells contribute to the clearance of amyloid-β plaques by engulfing and breaking down the protein. Glial cell dysfunctions in AD may therefore contribute to plaque buildup.
4. Synaptic function: Glial cells can regulate synaptic function by synaptic pruning, by recapture or release neuro- and gliotransmitters, or by providing targeted metabolic support. These essential glial functions, which contribute to the fine-tuning and proper adjustment of neuronal activity, may become dysfunctional in AD.
As a result, glial cells are increasingly considered promising targets for the development of therapies aiming at preventing the neuronal decline observed in AD.
The purpose of this research topic/special issue is to collect reviews and research papers addressing the function of glial cells during Alzheimer's disease in the domain of the four aforementioned functions along with prospective therapeutic strategies. Furthermore, we welcome papers on the potential role of glia cells in anti-amyloid therapies and related side effects.
1. Inflammation: In response to the buildup of protein aggregates such as amyloid-β plaques, glial cells become activated, release inflammatory cytokines, and send and receive complement-related signals, which together may exacerbate the damage caused by the plaques.
2. Neuroprotection: Glial cells, in particular astrocytes, provide neuroprotection by releasing metabolites, growth factors, and antioxidants, which help reduce oxidative stress and protect neurons in physiological conditions. In AD, these neuroprotective mechanisms are compromised, leading to excessive damage to neurons.
3. Clearance of protein aggregates: Glial cells contribute to the clearance of amyloid-β plaques by engulfing and breaking down the protein. Glial cell dysfunctions in AD may therefore contribute to plaque buildup.
4. Synaptic function: Glial cells can regulate synaptic function by synaptic pruning, by recapture or release neuro- and gliotransmitters, or by providing targeted metabolic support. These essential glial functions, which contribute to the fine-tuning and proper adjustment of neuronal activity, may become dysfunctional in AD.
As a result, glial cells are increasingly considered promising targets for the development of therapies aiming at preventing the neuronal decline observed in AD.
The purpose of this research topic/special issue is to collect reviews and research papers addressing the function of glial cells during Alzheimer's disease in the domain of the four aforementioned functions along with prospective therapeutic strategies. Furthermore, we welcome papers on the potential role of glia cells in anti-amyloid therapies and related side effects.
Keywords: Glial Cells, Alzheimer's Disease, protein aggregates, neuroprotection
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