2015
DOI: 10.1016/j.neuropharm.2014.08.012
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How dependent is synaptic plasticity on microglial phenotype?

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Cited by 22 publications
(11 citation statements)
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References 130 publications
(117 reference statements)
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“…Activated microglia and astrocytes can produce a significant range of soluble factors capable of modulating synaptic function and plasticity, such as inflammatory mediators, trophic factors, neurotransmitters and neuromodulators. Variations in the activation phenotypes of such glial cell populations is expected to translate into different capacities to modulate cognitive functions (Jones and Lynch, 2015; Patterson, 2015). Hence, hippocampal T cells infiltrating the brain in the context of tau pathology may directly modulate microglial and/or astrocytic activation status, towards a profile with detrimental impact on synaptic plasticity.…”
Section: Discussionmentioning
confidence: 99%
“…Activated microglia and astrocytes can produce a significant range of soluble factors capable of modulating synaptic function and plasticity, such as inflammatory mediators, trophic factors, neurotransmitters and neuromodulators. Variations in the activation phenotypes of such glial cell populations is expected to translate into different capacities to modulate cognitive functions (Jones and Lynch, 2015; Patterson, 2015). Hence, hippocampal T cells infiltrating the brain in the context of tau pathology may directly modulate microglial and/or astrocytic activation status, towards a profile with detrimental impact on synaptic plasticity.…”
Section: Discussionmentioning
confidence: 99%
“…Importantly, the cytoplasmic elongations of neurons and glial cells forming complex circuits have a deep functional relevance since their loss, or decrease, is involved in numerous neuropathologies [14,15].…”
Section: Introductionmentioning
confidence: 99%
“…Recent evidence suggests that failure of signaling required for maintaining a ‘resting’ microglial phenotype, likely important for preserving surveillance functions, might have profound consequences on synaptic activity. For instance, numerous studies have found that Aβ increases microglia activation and the release of cytokines which impair LTP, and that inhibiting microglia activation can prevent the block of LTP induction by Aβ (for a recent review see [138]). Further the loss of synapses, a hallmark feature of AD, has been linked to microglia phagocytic activity.…”
Section: Synaptoimmunological Dysregulation In Neurodegenerative/automentioning
confidence: 99%