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Microglial phagocytosis in aging and Alzheimer's disease
Enrique Gabandé-Rodríguez1, Lily Keane2, Melania Capasso2
1Department of Molecular Neuropathology, Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Madrid, Spain.
Abstract:
Microglia are the innate immune cells of the brain, which maintain homeostasis by constantly scanning and surveying the environment with their highly ramified processes. In order to exert this function, they need to phagocytose synapses as well as debris and dead cells, a process that is further amplified in pathological conditions. Importantly, it has been shown that microglia phagocytic capacity is altered in the course of neurodegenerative disease, for which aging is one of the highest risk factors. Thus, understanding how phagocytosis is impaired during aging is a priority for future research. Advances in this area are expected to significantly contribute to our understanding of normal cognition during aging, as well as changes that take place in age-associated neurodegenerative diseases. In this review, we will summarize the current knowledge on how phagocytosis is executed and affected by aging or in age-associated neurological disorders, such as Alzheimer's disease (AD). Furthermore, we will summarize both protective and deleterious consequences of altered phagocytosis in AD and where relevant in other neurodegenerative diseases.
Insights
Microglia, the brain's immune cells, perform essential phagocytosis. This review examines how aging impairs microglial phagocytosis, impacting neurodegenerative diseases like Alzheimer's disease.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia are the brain's resident immune cells, crucial for maintaining homeostasis through environmental surveying and phagocytosis.
- Phagocytosis by microglia involves clearing synapses, debris, and dead cells, a process vital for neuronal health.
- Microglial phagocytic capacity is known to be altered in aging and neurodegenerative diseases, including Alzheimer's disease (AD).
Purpose of the Study:
- To review the mechanisms of microglial phagocytosis.
- To explore how aging affects microglial phagocytic function.
- To summarize the role of altered phagocytosis in age-associated neurological disorders, particularly AD.
Main Methods:
- This review synthesizes current scientific literature.
- It examines existing research on microglial phagocytosis in aging and neurodegenerative contexts.
- The review discusses findings related to both beneficial and detrimental effects of phagocytosis alterations.
Main Results:
- Aging significantly impacts microglial phagocytic capabilities.
- Impaired phagocytosis in aging contributes to the pathology of neurodegenerative diseases.
- Altered phagocytosis in AD can have both protective and harmful consequences.
Conclusions:
- Understanding age-related changes in microglial phagocytosis is critical for neurodegenerative disease research.
- Targeting microglial phagocytosis may offer therapeutic strategies for aging and AD.
- Further research is needed to fully elucidate the complex role of phagocytosis in brain aging and disease.