In this review, we focus on the emerging roles of microglia in the brain, with particular attention to synaptic plasticity in health and disease. We present evidence that ramified microglia, classically believed to be “resting” (i.e., inactive), are instead strongly implicated in dynamic and plastic processes. Indeed, there is an intimate relationship between microglia and neurons at syn-apses which modulates activity‐dependent functional and structural plasticity through the release of cytokines and growth factors. These roles are indispensable to brain development and cognitive function. Therefore, approaches aimed at maintaining the ramified state of microglia might be crit-ical to ensure normal synaptic plasticity and cognition. On the other hand, inflammatory signals associated with Alzheimer’s disease are able to modify the ramified morphology of microglia, thus leading to synapse loss and dysfunction, as well as cognitive impairment. In this context, we high-light microglial TREM2 and CSF1R as emerging targets for disease‐modifying therapy in Alz-heimer’s disease (AD) and other neurodegenerative disorders.

Targeting microglia‐synapse interactions in alzheimer’s disease / Piccioni, G.; Mango, D.; Saidi, A.; Corbo, M.; Nistico, R.. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1661-6596. - 22:5(2021), pp. 1-17. [10.3390/ijms22052342]

Targeting microglia‐synapse interactions in alzheimer’s disease

Mango D.;Saidi A.;
2021

Abstract

In this review, we focus on the emerging roles of microglia in the brain, with particular attention to synaptic plasticity in health and disease. We present evidence that ramified microglia, classically believed to be “resting” (i.e., inactive), are instead strongly implicated in dynamic and plastic processes. Indeed, there is an intimate relationship between microglia and neurons at syn-apses which modulates activity‐dependent functional and structural plasticity through the release of cytokines and growth factors. These roles are indispensable to brain development and cognitive function. Therefore, approaches aimed at maintaining the ramified state of microglia might be crit-ical to ensure normal synaptic plasticity and cognition. On the other hand, inflammatory signals associated with Alzheimer’s disease are able to modify the ramified morphology of microglia, thus leading to synapse loss and dysfunction, as well as cognitive impairment. In this context, we high-light microglial TREM2 and CSF1R as emerging targets for disease‐modifying therapy in Alz-heimer’s disease (AD) and other neurodegenerative disorders.
2021
Alzheimer’s disease; Cytokines; Long‐term potentiation; Microglia; Neuroinflammation; Synaptic Plasticity; Alzheimer Disease; Animals; Humans; Inflammation; Membrane Glycoproteins; Microglia; Neuronal Plasticity; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor; Receptors, Immunologic; Synapses
01 Pubblicazione su rivista::01a Articolo in rivista
Targeting microglia‐synapse interactions in alzheimer’s disease / Piccioni, G.; Mango, D.; Saidi, A.; Corbo, M.; Nistico, R.. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1661-6596. - 22:5(2021), pp. 1-17. [10.3390/ijms22052342]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1620725
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