Microglial dyshomeostasis drives perineuronal net and synaptic loss in a CSF1R +/− mouse model of ALSP, which can be rescued via CSF1R inhibitors is a research paper published in Science Advances (2021). On theSindex it has a DataRank of 0. It has been cited 96 times.
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National Institutes of Health
Grant: R01NS083801
National Institute on Aging
Grant: R01AG056768
National Institute on Aging
Grant: U54 AG054349
National Institute on Aging
Grant: 1F31NS111882-01A1
Role of Microglia in Adult Onset Luekoencephalopathy with Axonal Spheroids and Pigmented Glia (ALSP)
National Institute of Neurological Disorders and Stroke
Grant: F31NS108611
National Institute of Neurological Disorders and Stroke
Grant: AARF-16-442762
NINDS NIH HHS
Grant: F31 NS111882
NIA NIH HHS
Grant: RF1 AG056768
National Institutes of Health
Grant: 1RF1AG056768-01A1
Microglia are necessary for cortical plaque formation in Alzheimer's disease
National Institutes of Health
Grant: 5R01NS083801-07
Origins, properties, and therapeutic potential of cells that repopulate the microglia-depleted adult brain
National Institutes of Health
Grant: 5R01LM013039-02
HealthyMe/MiSalud Smartphone Application: Identifying Mechanisms to Engage African Americans and Hispanics in Personal Health Libraries
National Institutes of Health
Grant: 5F31NS108611-02
Investigating the Role of Microglia in Huntington’s Disease
National Institutes of Health
Grant: 3U54AG054349-03S2
UC Irvine AD Translational Center for Disease Model Resources-Mini Microscope Technology Supplement
FWCI
7.09
Citation Percentile
1.0%
Citation Trend
Fields of Study
Keywords
Sustainable Development Goals
Additional file 2 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 2 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 3 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 3 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 4 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 4 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 5 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 5 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 6 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 6 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 7 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 7 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 8 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 8 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 9 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 9 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 10 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 10 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 11 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
Additional file 11 of A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques