Abstract：
:Microglia are brain-resident immune cells and regulate mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by a supernumerary chromosome 21, containing also genes related to the immune system. In the hippocampus of the Dp(16) mouse model of DS and DS individuals, we found activated microglia, as assessed by their morphology; activation markers; and, for DS mice, electrophysiological profile. Accordingly, we found increased pro-inflammatory cytokine levels and altered interferon signaling in Dp(16) hippocampi. DS mice also showed decreased spine density and activity of hippocampal neurons and hippocampus-dependent cognitive behavioral deficits. Depletion of defective microglia or treatment with a commonly used anti-inflammatory drug rescued the neuronal spine and activity impairments and cognitive deficits in juvenile Dp(16) mice. Our results suggest an involvement of microglia in Dp(16)-mouse cognitive deficits and identify a new potential therapeutic approach for cognitive disabilities in DS individuals.
journal_name
Neuronjournal_title
Neuronauthors
Pinto B,Morelli G,Rastogi M,Savardi A,Fumagalli A,Petretto A,Bartolucci M,Varea E,Catelani T,Contestabile A,Perlini LE,Cancedda Ldoi
10.1016/j.neuron.2020.09.010subject
Has Abstractpub_date
2020-12-09 00:00:00pages
887-904.e12issue
5eissn
0896-6273issn
1097-4199pii
S0896-6273(20)30710-8journal_volume
108pub_type
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